Ask Arthur … pretty much anything you like

Arthur’s done this all before. Hundreds of people around the world asked Arthur their questions about prostate cancer from 1994 to 1997 on the original Prostate Cancer InfoLink.

Please understand that Arthur is not a physician. He is only a reasonably well educated layman with some experience of prostate cancer and its problems. He cannot provide you with medical advice. You should always talk to your doctor about your clinical condition and how it should be managed.

You may post your question for Arthur using the comments/reply box below. Questions and answers are retained on this page for approximately 60-90 days from the time they are originally posted.

235 Responses

  1. Hi Arthur!

    Is it unusual for the pathology report to not include the length and Gleason score of the positive margins found? Where can I get this information if my pathology report doesn’t include this information? Also is it possible to get a second opinion on the entire specimen after RP to see if there were benign tissue at those margins identified as positive?


    Arthur responded as follows:

    Dear Mike:

    Arthur says that the quality of pathology reports can vary to a quite extraordinary degree, depending on the individual pathologist and the standards set and required by the organization/institution at which he or she works.

    Your first option is to see if it is possible to contact the pathologist who examined the original tissue and wrote the original report. However, if the report originally provided was of poor quality, the value of trying to contact the pathologist is at least open to question because he/she is going to be on the defensive from the get go.

    Arthur thinks a much better option would be to ask for the slides prepared from the original specimen to be sent to a recognized specialty prostate pathology center for a second opinion (which is perfectly possible and regularly done). Your urologist will need to assist you with this, however.

    Respected specialty pathology centers that can and do frequently provide “second opinion” services include the laboratory of Dr. Jonathon Epstein at Johns Hopkins in Baltimore, MD (click here for details); Bostwick Laboratories (click here for details); and OURLab (click here for details).

  2. I had EBRT about 3.5 years ago and my PSA went down to 1.36 ng/ml. My PSA today is 15.98 and I have been diagnosed with stage 2 cancer recurrence inside my prostate. What are your thoughts? Thanks,



    Arthur responded as follows:

    Dear Glenn:

    Arthur says that he has way more questions than answers. They start with whether you know your current PSA doubling time and they include other factors like your current age as well as your original PSA level, clinical stage, and biopsy-based Gleason score. They also include what your current doctor has been telling you while your PSA has been rising over the past 3 years!

    Arthur would suggest that your best best is probably to join the social network associated with this site, where they will work with you to try to get a clear understanding of your current risk level. It seems highly likely that you need additional treatment. The question is going to be what kind of treatment is appropriate and available. Salvage surgery can be carried out, but it is associated with a very high rate of complications and side effects. Salvage HIFU may be available in a clinical trial setting. Cryotherapy might be a possibility. Or you may be better of accepting that some form of hormone therapy (androgen deprivation therapy or ADT) will need to be the next step and working with your doctors to determine when that would be appropriate.

  3. Dear Arthur,

    Hello, I have written to you in the past regarding my husband’s T4 D1 prostate cancer. His initial PSA this past February was in the 800s and 900s, with Gleason 9 disease. Extensive regional lymph involvement was evident but no distant metastasis was found.

    His PSA went down to 320 ng/ml after IV antibiotics and down to 9.4 ng/ml after 2 weeks on Casodex therap. He is now finished with pelvic radiation (5 weeks ago) and has had two Lupron shots (each of 30 mg q4 months).

    Amazingly his PSA is stable at below 0.05 ng/ml. His serum testosterone is below 3. His alkaline phosphate is below 40. His doctors seem to be quite impressed. No side effects from radiation remain at present, although he did have them the last 3 weeks of treatment.

    He is mildly anemic and his liver enzymes slightly elevated (most likely from the Casodex). All other blood work is perfect. My question is: Would it be reasonable for me to ask the doctor for a Casodex-only vacation at this point (while he remains on Lupron). He does have some nausea and GI upset from the Casodex. We know he has to be on the Lupron for at least 2 more years. I can find no medical info on Casodex used intermittently.

    Thank You for your time,



    Arthur responded as follows:

    Hello again, Susan.

    So Arthur is perhaps not quite as surprised as you seem to be that you husband has responded well to the combination of radiation therapy and androgen deprivation. On the other hand, as always, Arthur is delighted to see such an apparently excellent response.

    Arthur further thinks it would be perfectly reasonable to ask your husband’s doctors whether it would be possible to stop the bicalutamide (Casodex) therapy, given the fact that there seem to be some significant potential side effects associated with this drug. The primary reason for the initial use of Casodex has been met (i.e., to prevent any flare reaction associated with the introduction of Lupron therapy). Having said that, there may be specific reasons why the doctors do believe your husband should be maintained on the Casodex, in which case you might want to ask whether a smaller or less frequent dose might be possible to alleviate the side effects.

    Let’s hope that your husband’s PSA is still down at < 0.1 ng/ml 2 years from now and that he is able to adjust well to therapy.

    Arthur also says, do make sure that he is sticking to a good, "heart healthy" diet and a regular exercise regimen to help alleviate some of the potential side effects of the ADT.

  4. Dear Arthur:

    Yes, thank you for your response. My husband eats an organic prostate cancer diet (set up for him by a prostate naturopath doctor). He does cheat once a week as recommended. We go back to the oncologist in November. I will ask about the Casodex then. Should I ask about having the ultrasensitive PSA done? Is below 0.05 (as stated on lab reports) enough information or should he be watched closer than that? The doctor’s office sends me the lab work results by e-mail, so I have not had the opportunity to ask this question. I will ask at next appointment.

    I appreciate your time.



    Dear Susan:

    By all means ask the oncologist about whether s/he is or isn’t using a sufficiently sensitive PSA test, but so long as your husband’s PSA is down below 0.05 ng/ml, that is certainly sufficient information.

    The other thing that Arthur would say is that a good oncologist would almost certainly be willing to discuss the Casodex issue over the phone if you ask for a brief phone call to explain the situation. If you ask for that phone call now, then it would give the oncologist time to think about this between now and the November visit, even if he or she isn’t ready to just let your husband stop the Casodex tomorrow.

  5. Dear Arthur,

    Yes after we spoke via this site, I did decide to call and asked if we could decrease dosage due to side effects. The call received back was from the NP who said doctor said to discontinue it and repeat blood work in 4 weeks instead of 8 weeks. They were very open-minded and responsive. I was given the impression that they respect outside research and input.

    This is the oncologist that I love. Such a different attitude than we were faced with in March with the urology branch of the practice, who were a bit different in their thinking.

    Thank you,



    Arthur responded as follows:

    Dear Susan:

    Arthur is pleased to have been of a little assistance … but you’re the one who did all the hard work!


  6. Dear Arthur:

    Thank you for your advice. It gave me the courage to trust my judgement after getting shot down on my last two suggestions to the urology and radiology branch of the practice. I just didn’t want to hear how serious his situation was again. We heard it and understood it the first time in March. We feel better all around now.


  7. Having read all the comments I’m a lot better informed. Will have myself checked as soon as.

  8. Dear Arthur,

    My dad (who is in his mid 80s) is scheduled to undergo prostate biopsy in 2 days. His PSA is almost 70; he has been on two prostate medications (Proscar and doxazocin) for the last 10 years. My dad is an angina patient, and is extremely sensitive to pain. Is there anything you would recommend we ask the doctor to provide before the biopsy to help with the pain?

    Isn’t there an injectable anesthetic that might be more helpful to block the pain? Or anything else to help with the pain.

    The doctor has only recommended he take Valium to help relax before the procedure.

    I really appreciate your help and time.

    Thank you,
    Green girl


    Arthur responded as follows:

    Dear Green Girl:

    Arthur says you might want to check with the doctor whether he intends to give your father local anesthesia with lidocaine at the time of the biopsy procedure. This is now commonplace and is described in detail in this article on the Medscape web site. (You do need to sign up for Medscape to see the article, but it’s free and you don’t have to be barraged with junk e-mail.)

    Arthur also says that if the urologist is not used to doing this, then your Dad does not want to be the first patient he tries this on! If the current urologist has no experience of giving local anesthesia for prostate biopsies, can you get a referral to another urologist?

    Third, Arthur would note that you need to be very cautious about what your Dad wants to do if he is found to have some prostate cancer on biopsy. Many of the available treatments for localized disease may not be appropriate for an 80-year-old man with angina. Arthur thinks that before he did anything — if he was wearing your Dad’s shoes, and someone found some cancer in his prostate at 80 years of age with a PSA of 70 ng/ml — Arthur would want to get a bone scan done to see if there was any sign of disseminated prostate cancer. There very probably is not, but it would be a wise precaution before making any other decisions.

  9. Dear Arthur,

    I had a TURP on December 16, 2011. There was no cancer. In November 2012 I had PSA of 2.0, and this week I had a PSA of 3.5. What I should do now?

    Please help.



    Arthur responded as follows:

    Dear Nasser:

    Arthur says that he has no good answer to your question because you haven’t provided enough information. Arthur would need to know all of the following to be able to offer a helpful answer to your question:

    — Your age
    — Whether you have any family history of prostate cancer
    — Whether you have or have had any symptoms of urinary tract problems since your original TURP
    — Whether your doctor can “feel anything” like a lump or hard spot on your prostate when he gives you a physical examination

    Is is possible that you need a biopsy? Yes, it is. It is certain? No, it is not. You could have a rising PSA fpor all sorts of possible reasons.

    The sensible thing for you to do is to go and talk to your urologist and get his opinion rather than Arthur’s! Your urologist will be able to actually examine you and answer your questions for you in a much more informed way that Arthur possibly can.

  10. Hi Arthur,

    I am 15 months post RP and my PSA has been low and stable around 0.030 using the ultrasensitive assay (LDL 0.014) until the last test came back at 0.040. Is this increase significant? Could this be a lab error? It has me a little nervous. Where do I go from here? Is it time to consider secondary treatment?


    Arthur responded as follows:


    Arthur says that a single, tiny PSA blip like this really shouldn’t be any cause for worry. It is well within the margins of error of the ultrasensitive PSA test, and so you can’t have any confidence in its clinical significance. Your next PSA could equally easily come back at a value of (say) 0.025 ng/ml. So the sensible thing is to try and “chill out” until you have your next PSA test is due (although Arthur is well aware that that is easier to say than to do!).

    Arthur does note that you could, if you want to, talk to your urologist about having your next PSA in 2 months time as opposed to 3 months. This would be one way to abbreviate the period of stress.

    Arthur is sure that your urologist has already told you that there is no need to get overly anxious at this point in time. Even if your next PSA level was to come back at 0.050 ng/ml in 3 months time, the really critical question to be considered would be the rate at which your PSA is doubling if it does start to go up slowly like this. That would help to determine what any next treatment might need to be (if further treatment does prove to be needed — which it may well not).

  11. Hi Arthur,

    Because of my PSA results were detectable at 0.030-0.040 ng/ml (15 months post-RP) using the ultrasensitive assay (LDL 0.014), my urologist had me take a CT scan of my pelvic and abdominal area. The only thing found was kidney stones; no sign of cancer spread. My question to you is, what did he expect to find with my PSA being at such a low level? Is it possible to find anything at such a low level?


    Arthur responded as follows:

    Dear Orson:

    Arthur says that you would need to ask your urologist what he thought he might be able to find with a CT scan at that PSA level. All that Arthur is able to tell you is that the people at the Mayo Clinic in Rochester, MN, will only give patients a choline-11 PET/CT scan post-RP if their PSA has risen to at least 0.2 ng/ml (i.e., something like five times higher than yours). We do know that choline-11 PET/CT scans are significantly more sensitive than a standard CT scan.

    It is possible that your urologist had a “non-standard” reason for giving you a CT scan (because of course Arthur doesn’t have all of the relavant information), but Arthur has no idea what that might be.

  12. Hi Arthur.

    With the advice of my urologist I have an appointment today with a radiation oncologist about my stable, low but detectable PSA (0.030-0.040 ng/ml) 15 months post-RP. This is a new journey for me, so, if possible, please give me at least 3 important questions to ask the oncologist at my consultation?


    Arthur responded as follows:

    Q1: I understand that this is a very small rise in my very low PSA level, and based on a single test result at this time. In order to minimize risk for over-treatment, wouldn’t I be wise to get at least one more repeat PSA test before actually committing to any form of second-line treatment?

    Q2: If I decide to defer any second-line therapy until I get a repeat PSA test, what PSA level would make you think I really did need to get immediate treatment as opposed to waiting. I mean, what if the next PSA test result 3 months from the last one just came back at 0.040 ng/ml again?

    Q3: If radiation does prove to be needed, what do we need to do to be able to make really good decisions about what areas might need to be radiated? My current understanding is that there is no available imaging test — even PET/CT scanning — that could accurately identify an area of recurrence of my cancer based on the current PSA level. Is that right?

    Q4: If we are unable to identify a specific area of recurrence, but my PSA was to rise again to (say) 0.060 ng/ml when I got another PSA test done, how would you suggest we moved forward? What area(s) would you think it would be wise to radiate? And would you think it was wise to combine that radiation with a brief course of androgen deprivation therapy?

  13. Hi Arthur.

    I had the consultation with the radiation oncologist and I really didn’t expect to get his unbiased opinion. His reasons were the same reasons as my urologist’s for recommending secondary treatment now as opposed to waiting, even though I’m 15 months post-surgery with a low, stable, but detectable PSA of 0.030-0.040 ng/ml.

    Their three reasons are: (1) I’m age 43 years; (2) the Gleason score of 3 + 4 and the stage pT2c; (3) one focal positive margin, even though the Gleason grade was only 3 at the margin.

    I told them I’m willing to wait and see what the results are for at least two more PSA tests (2-3 months apart) before making that decision. I need some guidance. Please help!


    Arthur responded as follows:

    Dear Mike:

    Please understand that Arthur cannot tell you what to do. In the end this is about what you want to do in consultation with your physicians.

    Arthur can only point out the obvious, as follows:

    (1) It is a lot easier for your doctors to tell you get treatment now than it is for them to suggest that you wait for a little while. If they treat you now, they know that they have taken immediate action to ensure that the disease doesn’t progress. They will also have increased your risk for complications and long-term side effects of treatment, but in their minds they may have “saved your life”.

    (2) If you wait for another few weeks to get at least one more PSA test and then make a decision, your cancer could, certainly, progress. However, if you don’t wait for another few weeks to get another PSA test, and you get immediate treatment, you are never going to be sure that that treatment was really necessary, and then you could end up second-guessing your decision.

    (3) Your doctors are giving you their unbiased opinions from their perspectives. The problem is that they don’t have your perspective, … and nor can Arthur.

    Arthur fully appreciates that you are in a very difficult position. Others have been here before you, and still others will be here after you. There is no “right” or “wrong” here. There is only what you feel comfortable doing. If you get another PSA test in a few weeks time and it is somewhere north of 0.070 ng/ml, then there will clearly be good reason to go ahead with second-line therapy. The question is not what you do in a few weeks time. It is what you want to do now.

  14. Hi Arthur.

    Could you please give me the meaning of this finding from my final pathothology report (John Hopkins):

    “The right anterior margin close to apex is positive where we cannot determine whether it is an area of intraprostatic incision or extraprostatic extension due to ambiguities of the histologic boundary of the prostate in this region”; Gleason 3 + 3. Does this mean I have aggressive cancer?


    Arthur responded as follows:

    Dear Orson:

    Arthur says, no, this does not mean that you have aggressive cancer if all your cancer is Gleason 3 + 3 = 6. It means that there was an area at the “apex” (the lower end) of the prostate where there was a clear indication that there was cancer right at the very edge of the surgically removed specimen. This does not mean it is aggressive, but it does mean that there might have been a tiny amount of cancerous tissue left behind by the surgeon. This may or may not prove to be important over time, and you need to discuss this finding with your surgeon because obviously Arthur does not have all the details.

    Arthur would also tell you that the incidence of small amounts of surgical margin disease are not uncommon, particularly at the apex of the prostate, which is associated with the greatest degree of difficulty for the surgeon in being sure that s/he has excised all of the relevant tissue. Such small, positive surgical margins, when they are of low grade (i.e., Gleason pattern 3) are not usually a significant clinical issue, and the surgeon may actually have removed all of the cancerous tissue anyway. The problems tend to arise when the surgical margins are larger or multi-focal and/or are of high Gleason patters (e.g., 4 or 5).

  15. Wonder if you could review the article below and provide comment:




    Arthur responded as follows:

    Dear AKAI:

    Arthur says he thinks you will find what you are looking for if you simply click here. The sitemaster commented on this paper when it was initially published.

  16. Arthur … Are you aware of or have any comments about the FDA Phase II trial of GenEpic’s supplement for prostate cancer (see


    Arthur responded as follows:

    Dear John:

    Arthur says no, he was not aware of this trial. The only other thing he can say at this time is that this trial is not listed on the web site, which would be a necessary requirement for almost any clinical trial that was to be taken seriously by the FDA. Indeed, no trial of the GeneEpic supplement appears to be listed on the web site.

  17. Hi Arthur.

    Is it common to still have seminal fluid released during sexual intercourse after your prostate has been removed, along with the seminal vesicles? If so does this mean the surgeon left something (prostate tissue, etc.) behind which would cause a slight increase in your PSA reading after sexual intercourse? I thought if these organs were completely removed you could only experience a dry orgasm.


    Arthur responded as follows:

    Dear Mike:

    It seems extremely unlikely to Arthur that any fluid that is being expelled at orgasm after a full radical prostatectomy is actually seminal fluid. However, some men do continue to expel other types of fluid at orgasm after a radical prostatectomy, most commonly a small amount of urine (i.e., “climacturia”).

    Arthur says that you might like to look at this extensive discussion of orgasm after RP that you can find on the HealingWell web site.

  18. Arthur:

    This is clear sticky fluid (semen) not urine being released. It’s not a lot but it’s enough to where it’s noticeable. What could be the reason this is happening?


    Dear Mike:

    Arthur is not urogenital physiologist. You are going to need to talk to your urologist about this, but what Arthur does know is that a man with no prostate is unable to produce semen. It may feel like semen, but as far as Arthur is aware there is no way that it can be.

  19. I am 8 months post-prostatectomy and also have viscous secretions during sexual activity. I assume that these secretions come from the Cowper’s glands which remain intact after prostatectomy. Normally, these secretions are the pre-ejaculate and act as a lubricant. The Cowper’s glands may also produce some PSA.


    Arthur responded as follows:

    Thank you Ray. That is a very helpful piece of information that (in retrospect) Arthur thinks he may have heard once before but had entirely forgotten. (Arthur, like his readers, isn’t getting any younger!)

  20. Hi Arthur,

    My father was diagnosed with prostate cancer late October/early December. His PSA level was 18.9 at the time and his Gleason score was a 9. He is 58 years old and currently residing in Victoria. After his biopsy his prostate was found to be enlarged with a tumour. After doing a PET scan and MRI, it was found to have also spread to his pelvis bone. There is also suspicion it has spread to his hips but this cannot be confirmed.

    We were advised there is no cure and one doctor has told him life expectancy is 18 months. Another doctor who is much more optimistic has told him it is generally 2 years given that the hormone treatment he is on currently fails and chemo, which is the plan at this stage later down the track, also fails. BUT life expectancy can also be up to 10 years. The second doctor has also told him to be optimistic as there are lots of new drugs on the market.

    My father has now become quite depressed after hearing the news that he could only be alive for another 2 years, constantly reminding us that he wants to live to see his grandkids born. This is painful to hear. Can you provide your insights on life expectancy, and quality of life, for people in his situation? Also we were advised that chemotherapy could be preferred over radiotherapy given the spread of the cancer being uncertain. Do you believe this is the right treatment option?

    He just had his first hormone injection this week and has another medication which is tablet form he now takes daily. We were told to bring him in for a blood test in 3 months time to monitor his progress.

    Kind Regards,



    Arthur responded as follows:

    Dear Melanie:

    Arthur says he is sorry to hear about your father’s diagnosis. He clearly does have a relatively aggressive form of prostate cancer that has already metastasized. However, making individual assessments about life expectancy for individual patients is extremely difficult. Arthur is aware of men like you father who were, indeed, dead within 18 months to 2 years. He is also aware of men like your father that were still alive at 10 years or more. So much depends on the response of the individual patient to available forms of treatment, starting with the androgen deprivation therapy that he is already receiving.

    There are three things that Arthur knows about dealing with situations like this:

    (1) If your father is going to just accept the idea that he will be dead within 2 years, then he is doing himself no favors, and he may well be encouraging a self-fulfilling prophecy. Somehow you are going to need him to focus on the other thing he was told — that 10 years and more is not impossible and that there really are a LOT of new drugs that have recently come available and there are more on the way.

    (2) He needs to get himself to the best prostate cancer he can get to in Victoria, i.e., one where there are several physicians who really specialize in the management of late stage prostate cancer and understand how to optimize patient survival and the patient’s quality of life too.

    (3) He needs to talk to these physicians about getting involved (as and when appropriate) in clinical trials of the new drugs that are in development so that he is “ahead of the curve”, and not just a passive recipient of whatever form of treatment his doctor thinks would be appropriate when the earlier treatment has failed.

    And there is another thing that is harder to say, but Arthur needs to say it anyway … It is not fair of him to try to “blackmail” you over the grandchild issue. The way Arthur would deal with this is to tell him that if he wants to live to see some grandkids, he’d better d*** well be around to play with them as they are growing up because if there are going to be grandkids, his job it to be around long enough for them to be able to remember playing with him! The corollary is, “So Dad, stop whining and start doing something about living for 10+ years as opposed to just two!”

    How your father adapts himself to the changed circumstances is going to be critical to what everyone can get out of this situation — whether it is for 2 years or 20. Arthur says it’s OK for him to be depressed and angry for a while. It’s part of the journey. But sooner or later (and better sooner) he needs to decide that he isn’t going to just roll over and let this happen to him. His attitude and his actions are going affect the lives of all those around him … potential grandkids included.

  21. Arthur, I hope you can convey the following to Melanie.

    I, too, am 58. I, too, have Gleason 9 prostate cancer that has metastasized. I, too, had my heart sink when I read, in a well-known, widely respected book written by a world-class physician, that ADT (androgen deprivation therapy) would be effective for only about 18 months before my cancer became castration-resistant.

    I’m guessing that Melanie’s father took in the same news that I did, but may have failed to pay attention to several crucially important points:

    1. That particular eminent physician wrote his book more than 20 years ago. He was a surgeon, not an oncologist. The section on hormone ablation has been revised slightly in the subsequent editions, but it was already badly out of date 15 years ago. Today, no reputable physician who is conversant with the current state of the art would claim that the average length of effectiveness of ADT is only 18 months. The more you know — and there’s a LOT to know — the greater ability you have to play the cards you were dealt, not the ones you wish had been dealt.

    2. The term “average” has a technical meaning — actually, unfortunately, several technical meanings — and its meaning derives only from groups, not any one individual. To stake your future happiness on one number, the “average”, is insufficient and sometimes absurd. (“On average, an adult human being has one mammary gland and one testicle.”)

    In Melanie’s father’s case, even if the “18 months” represented a useful fact about some group of men (which it might very well not do; see point #1) it absolutely does not mean that anything in particular happens at the 18-month mark. The data set used to compute this average includes men whose PSA was in the thousands at start of treatment and who died within a few weeks. It also includes men who lived on for many decades.

    Almost certainly, most of the men in the group whose average was measured were men much older than Melanie’s father, and who lived and died many years ago. Are they representative of 58-year-olds in 2013? Probably not.

    3. More on “average”: We usually expect the average to be the “mean” — that is, the value most representative of the aggregate when summed together and divided by the number in the group. However, in many medical uses, the term “average” is used for the “median” — that is, the value where half of the group are below and half are above. The median is much easier to measure in a distribution with a long right tail, such as a group where a substantial number die within a couple of years but some go on to live for 20, 30, 40, or more years. In such a distribution (which is quite usual for many diseases and treatments), there is no way to compute the mean until several decades pass, and so the median is used instead. Melanie’s father’s goal is to get well to the right side of the median. Once he’s there, his mean life expectancy will not be hugely shorter than that of 60-year-old Australian men generally.

    4. Suppose ADT remains effective for only N months, where N = 18 or any other value. Nowadays, there are plenty of agents that continue to keep symptoms at bay that have very tolerable side effects. Although none so far have been shown to be curative, staying alive for another 5 or 6 years might well get this gentleman to a place where even more agents keep him alive, and even fairly healthy, for another 4 or 5 years; and during that second period of 4 or 5 years, even more agents will be developed such that (etc., etc.).

    Yes, the series of postponements does converge. We all must die at some point. And that leads me to …

    5. Melanie’s father has the same choice about how to live the rest of his days as we all do. All of us on Earth have the same horizon, and the west-bound sun: for some of us the horizon is farther, for others closer; the sun is higher or lower in the sky depending on our situation. We can curse the approaching darkness or make merry in the light that remains.

    Having said all that, my heart goes out to Melanie’s father. When I was diagnosed in 2007, my daughter and her husband-to-be postponed their previous plans to move away and start new careers a long way away. After a few months of shock, and initial treatment failure, they had a choice to follow their dreams or to stick around me. They made the choice that I hoped they’d make, and have found success in their careers far from home.

    Several years later, on their own timeline and not anyone else’s, they decided to start a family.

    Less than a month ago, I made it to the second of the milestones I had set for myself back in 2007 — I held my beautiful grandchild in my arms. Therefore, what Arthur said truly resonates with me; my next milestone is to leave an indelible impression on my grandkid. I expect it to take a while ….


    Arthur responded as follows:

    Thank you, Paul, for your very clear and “personal-experience-based” insights. Arthur has asked the site master to make sure that Melanie knows about this message.

  22. Dear Melanie/Arthur,

    I have written to Arthur several times regarding my husband Paul who has Stage 4, Gleason 9 prostate cancer. We too were told by four specialists the 18-month to 4-year numbers. I spent the next 6 months reading every medical study I could get my hands on and found this to be mostly untrue. My husband is now only 8 months into treatment but is in total remission and symptom free. His PSA was 928! His present PSA is undetectable!

    We decided if medical science could only offer us so much at present we could do the rest on our own and stay alive until medicine irons out the kinks in the latest treatments. First of all, only God knows how long any of us have, not medicine. I am a medical professional myself and have seen predictions be way off. It is a proven scientific fact that a positive attitude encourages longevity. We have control over our bodies more than medical science does.

    My husband is 61, works full time at a demanding job, and is enjoying his two new grandchildren, and the other 3 born a few years ago. He has changed his diet and added supplements I have researched extensively. At his last visit with our present oncologist (whom we love) his prognosis was changed from terminal to intent to cure! No promises, but being treated with a different attitude. His last two doctors old me I am probably more informed than they are (with regard to alternative treatment) and were asking me what I was giving him. Radiation treatment has improved dramatically in the past 5 years even for cancer in the bones.

    Do not let your father give up! We have our eyes on the 10-year mark right now. And if we are wrong and my husband becomes ill in 5 years, he has been happy and lived life to the fullest. Why be miserable waiting for something to happen that may not. Take charge! Once you get over the shock … and you will … put it on a back shelf. It is not the number of breaths you take, it is the number that take your breath away. Be hopeful. Plan a vacation!



    Arthur responded as follows:

    Dear Susan:

    Arthur says, thanks for the additional input for Melanie and her Dad … and Arthur is very glad to hear that you and your husband are both doing so well.

  23. Well said … I was diagnosed with metastatic disease nearly 12 years ago and and still going strong despite dire prognosis from my oncologist … In fact, in that time I have had three of my friends pass away, one from pancreatic cancer, one from a heart attack, and one from a swimming accident all of whom were concerned and praying for me!

    Ignore the prediction as statistics can be misleading for an individual. However, educate yourself about prostate cancer to become an empowered patient. Take steps to change your lifestyle, eating healthier and exercising regularly to enhance your body’s chances
    to slow the disease progression. And, most important, enjoy every day.

  24. Dear Arthur,

    I have written to you before but, to refresh everything: I had a robotic assisted prostatectomy in November 2011, following positive biopsies and PSA of 5.8.

    Post surgical report: stage T2c, Gleason 3 + 4, no extensions, but a positive margin. My post-op PSAs were non-detectable till now, but the most recent result is 0.04 ng/ml.

    My urologist recommends waiting and re-testing in 3 months. My question is: Isn’t that too late? And does this not really mean that there is a definite recurrence? Then are there any statistics on what my chances are? What should be the next step? What else can I do meanwhile. I had not altered my lifestyle and diet. Will that make a difference? And what regimen do you recommend.

    I am 51 years old and otherwise in excellent health.




    Arthur responded as follows:

    Dear Abbas:

    Athur says that a single PSA value of 0.04 after previously “undetectable” PSA readings could be a consequence of all sorts of things. For example, the test could have been done using a different type of PSA test, or at a different laboratory, or all your previous tests could have been about 0.04 ng/ml but reported as “undetectable” because any result lower than 0.1 ng/ml is classically defined as “undetectable”.

    Arthur thinks that you should listen to your urologist and see what your PSA is in another 3 months. However, if you are really, really worried about this, maybe he will “do a deal” with you and give you a repeat test in another 2 months rather than 3. There are may reasons to think that your next PSA will come back as 0.04 again, or perhaps even lower.

    The one thing you might want to ask the urologist is whether your most recent PSA value was carried out using the same PSA test type and at the same laboratory. If a different PSA test type was used, or the test was done at a different laboratory, there is a very high probability that that would explain the change in your report.

    Arthur does not think you need to “do” anything at this point in time. Recurrence at a PSA value of less than 0.2 ng/ml is defined by at least two increases in the PSA value (not just one).

  25. Dear Arthur,

    I have learned that math miscommunication is very common, and that whenever a result is unusual (not here) or there is a concern over a result thought to be unusual (as here), I would urge double-checking the figures and putting them in context.

    You correctly pointed out that the term “undetectable” has undergone a shift in meaning, and now means “less than 0.1 ng/ml, regardless of detectability”. (Why? In the 1990s, values < 0.1 could not be detected by then-current technology. The word was unfortunately retained even though the technology advanced.)

    Therefore, if Abbas's reporting is correct, nothing at all has happened to his PSA, so far as anyone can tell. His PSA has continued to be "undetectable", without any cause for concern, ever since his primary treatment. If his figure of 0.04 is accurate, then his doctor should have told him this: "Your PSA still remains at 'undetectable' levels, defined as < 0.1 ng/ml. Since there is no evidence whatsoever of recurrence, there is no reason to do anything different."

    Example: If the figures are as reported, his four PSA readings since November 2011 could have been reported in either of two ways:

    A. (Interpretation only): "negligible / negligible / negligible / negligible"
    B. (Observation only): "0.06 / 0.03 / 0.07 / 0.04"

    In either case, nothing of significance has occurred; every value is equal to 0.05 ± 0.03 ng/ml, indicative of no disease. But a change in communication style — from interpretation to observation for the fourth value only — might have caused a miscommunication.

    However, intercommunication between patients and doctors and labs has been known to get the decimal point wrong. For example, a PSA of "0.4" might be informally pronounced as "oh point four", misremembered as "point oh four", written down as ".04", and then slightly edited to "0.04". If this is what actually happened, then it would explain why there might be some concern.


    Arthur commented as follows:

    Correct. All true!

  26. Thanks so much Arthur, as usual you are a great source of information and wisdom. The test was done at the same lab and using the same method.



  27. Thanks Paul and Arthur, I appreciate you guys informing me and at the same time putting my mind at ease a little.

    I checked with the nurse. According to her, all my previous six readings (last one in July 13) have been under 0.04 (they do not report the value of anything under 0.04; they report it as non-detectable in their system) and the new January 14 one is exactly 0.04, all done in the same laboratory using the same method.




    Arthur responded as follows:

    In that case, Abbas, Arthur doesn’t think you should consider the single 0.04 ng/ml reading in January to be a clinically significant change in value. However, you do need to keep a close eye on follow-up PSA values. If they continue to rise, then there is clearly an issue of some form. You may also want to tell your doctor that you want another test done after 3 months as opposed to 6 months.

  28. Hi Arthur,

    My PSA has started to rise after 2 years on abiraterone + prednisolone. It’s been suggested to me that changing the steroid to dexamethasone could help. I can’t find anything that supports this — only that adding dexamethasone to abiraterone helps when no other steroid is being used. Have you heard anything about this?



    Arthur responded as follows:

    Dear David:

    Arthur is not aware of any specific trial that has demonstrated a positive result from switching patients who have a rising PSA on abiraterone + prednisone or prednisolone to abiraterone + dexamethasone.

    Having said that, Arthur certainly doesn’t think there is a lot to lose from trying such a strategy. If your PSA was to stabilize or go down again, that would be good. If your PSA continues to rise, then nothing would have changed.

    You should be aware that the two earliest trials of abiraterone to treat men with metastatic CRPC actually used it in combination with dexamethasone as opposed to prednisone/prednisolone, and Arthur was somewhat surprised to see prednisone or prednisolone get substituted for dexamethasone when the Phase III trials were implemented some years ago. It seems that most of those involved with the trial designs felt much more comfortable using prednisone/prednisolone than dexamethasone.

    The one question that Arthur would raise with the doctors if he was in your shoes would be “What dose of dexamethasone?” Dexamethasone is a stronger corticosteroid than prednisone, and so it can have more significant side effects. Arthur would want to ask the doctors what they thought the lowest appropriate dose of dexamethasone might be to start at.

    For comparative purposes, Arthur notes that, some time ago now, it was shown by Rajkumar et al. that low-dose dexamethasone was actually better than high-dose dexamethasone when combined with lenalidomide (Revlimid) in the treatment of patients with multiple myeloma.

  29. Hi Arthur. What caused decrease in PSA?

    I’m 17 months post-surgery. My PSA result from October 2013 was 0.040 ng/ml using the ultrasensitive PSA test. Well my latest result was 0.033 ng/ml. My urologist was talking radiation (I had a positive surgical margin, with Gleason 3 at the margin) because of the 0.040 result from October but now that it has decreased, what am I to do next? Should I radiate anyway?


    Arthur responded as follows:

    Dear Steve:

    Arthur says that you appear to offer a clear case study for why it is not such a good idea to make decisions about things like salvage radiation therapy on the basis of a single ultrasensitive PSA result.

    The first issue, of course, is what your PSA was before you got the reading of 0.040 ng/ml last October. A result of 0.040 ng/ml is still extremely low, and few urologists of Arthur’s acquaintance would actually suggest immediate salvage radiation therapy on the basis of that single result, which might have occurred for a dozen different reasons, starting with laboratory error.

    The fact that your PSA has now dropped down to 0.033 appears to suggest there is no necessity for any panic at all. You probably should simply talk to your urologist about getting another PSA test in another 3 months’ time. If the next one comes back no higher than 0.040 ng/ml, Arthur still wouldn’t see the need to do anything. Lots of men have a positive surgical margin. Sometimes it is clinically significant; sometimes it isn’t. On the other hand, if the next one came back at 0.050 ng/ml, then you might want to open that conversation with the urologist again about the wisdom of salvage radiation therapy.

    However, Arthur is not your doctor. You need to discuss the situation with him/her in a calm and rational manner. Patients often tend to over-react to a single PSA result. The sensible thing is usually to say, ‘Let’s get another one in a month, or 2 month’s time, and see if there is a nything “real” going on here before we make any rush to judgment.’

  30. Arthur:

    My PSA results before the 0.040 result were 0.028, 0.030, and 0.030, then the 0.040 and 0.033, all using the ultrasensitive PSA test; the first two results (3 months apart) right after surgery were < 0.050 using the standard PSA test.

    I don't see any evidence of a doubling time or an upward trend to warrant radiation right away! Is it out of the question to suggest that we keep watching my PSA say every 2 months and, if the are any significant changes (say if it doubles or increases to 0.070), then maybe radiation? Right now it is low and stable 17 months post-surgery, even with the positive margin.


    Arthur responded as follows:


    Arthur can’t see any justification for salvage radiation therapy at this time based on the numbers you have provided. He’s not even sure that anyone could reasonably argue that there has been a meaningful change in your PSA level at all.

    Arthur would also point out that a possible explanation for the tiny increase in your PSA over 17 months could be that your surgeon left some normal (non-cancerous) prostate tissue behind at the time of surgery. This can happen. If he did, that remaining normal tissue might have grown slightly and could be the cause of the very small increase in your PSA.

    In Arthur’s opinion, it would be perfectly reasonable to just go on getting your PSA taken every 3 months. However, if you are going to feel more comfortable getting the PSA every 2 months, then by all means talk to your urologist about this, but Arthur really doesn’t see anything in your data to suggest that this is necessary. He thinks that a lot of what is going on her is (quite understandably) “in your head” rather than in your prostate.

  31. Hello Arthur: my husband Don who is 90 years old has Methastatic prostate cancer to the bone and no bone pain right now. He had Lupron for a year and then stop working. Then he had chemotherapy or Docetaxel but had very bad side effects so only took a dosis. He is thinking about having Xdandi but does not like the possible side effects. He would like to know if he does not follow any treatment what are the symptoms that he may experience as the cancer advances?

    Thank you for your answer.



    Dear Nidia:

    Arthur says he is aware that the sitemaster has already posted an answer to your husband’s original question to Dr. Krongrad that Arthur would tend to agree with (just click here to see that answer).

  32. When are positive margins insignificant or significant? We all know that positive margins are an adverse finding on the path report after prostate surgery but do they always result in BCR?


    Arthur responded as follows:

    Dear Ron:

    Arthur says that interpreting when positive margins are significant or insignificant is an art, not a science.

    The best guidance that Arthur can give you is that a very small positive margin (say 1-2 mm long) that is Gleason pattern 3 in a man who had Gleason 3 + 3 or Gleason 3 + 4 disease has a lower likelihood of being significant and, conversely, a larger positive margin that is Gleason pattern 4 or 5 in a man who had Gleason 4+ 3 = 7 disease or higher (i.e., Gleason 8, 9 or 10) has a much higher likelihood of being significant. However, a bunch of other factors may also be important, and every case has to be considered on it’s individual merits.

    Arthur is sorry that he can’t be more specific, but your question is one that even specialists who have spent years studying issues like this can’t give you (or Arthur) a perfect answer to.

  33. I respectfully suggest, Arthur, that you may have over-answered this.

    Q1. (When are positive margins significant?)
    A1. Positive margins are always significant, because the finding indicates a higher level of risk than negative margins would have done.

    Q2. (Do positive margins always result in BCR?)
    No. There are some men, likely thousands, possibly tens of thousands, whose pathology report says “positive margins” but who never progress to biochemical recurrence.


    Arthur responded as follows:

    Dear Paul:

    Arthur thanks you for your comment, which is entirely appropriate. In his self-defense, Arthur would only note that he was trying to give an answer which might offer some specific additional insight for the individual asking the question.

  34. Hi Arthur.

    What is causing these fluctuating PSA results?

    Surgery on August 16, 2012. Subsequent PSA results: < 0.05, < 0.05 undetectable standard psa test, then 0.028, 0.030, 0.030, 0.040, 0.033, 0.038 detectable using the ultrasensitive PSA test!

    Is this up and down fluctuation a good enough reason to go ahead and start radiation? All of the tests were at least 3 months apart!


    Arthur responded as follows:

    Dear Tim:

    Arthur would respectfully suggest to you that this sort of variation in your PSA levels is well within the normal level of laboratory variance for what are, to all intents and purposes, “undetectable” PSA levels. These types of test simply do not have the sort of consistent level of accuracy that you seem to think they have. Arthur looks at these data as simply telling you that ever since your treatment, you PSA level has been < 0.05 ng/ml, and that is an excellent result.

    Furthermore, even if your PSA has risen by a tiny amount in the past 18 months (i.e., from 0.028 to 0.038 ng/ml), this could be a consequence of re-growth of some small amount of normal prostate tissue left behind at the time of surgery, and not have anything to do with cancer.

    In all honesty, Arthur thinks that you are over-reacting to these numbers. If we didn't have an ultrasensitive PSA test, an old-fashioned, standard PSA test would have told you that you consistently had PSA levels of < 0.1 ng/ml and you would be a very happy camper.

    If your PSA level was to suddenly jump to 0.08 and then to 0.10 ng/ml, the situation would be different, but as of now, if Arthur was in your shoes, there is no way he would be even thinking about salvage radiation therapy based on these data.

  35. Should we radiate anyway when there are positive margins?

    With positive margins being an adverse finding on the pathology report should we radiate anyway, regardless of favorable Gleason grade at positive margin, length of positive margin, or total Gleason grade?


    Arthur responded as follows:

    Dear Charles (or are you also Tim?):

    Arthur says that there is no absolute rule stating that every patient with a positive surgical margin needs to have immediate adjuvant radiation therapy. Every case has to be considered as exactly that — an individual case, on its merits. The decision as to the value of follow-up radiation treatment depends on all sorts of things, including the Gleason pattern of the tissue at the positive margin, the size of the positive margin, the patient’s post-surgical PSA levels and PSA doubling time, the patient’s age, etc.

    Arthur would note that one also has to bear in mind that adjuvant and salvage radiation therapy both come with risks for side effects and complications. Skilled physicians will try to ensure a balance of risks and benefits by not unnecessarily over-treating men in whom a small positive margin may have been present (but is showing little to no sign of post-surgical progression) while similarly ensuring sufficiently early treatment of men with a positive margin (or margins) that suggest or indicate a significant risk for progression.

    In Arthur’s experience, it is far from unusual for men with a small positive margin (especially one of low grade) to go for many years — or for the rest of their lives — without any sign of disease progression or any consequent need for radiation therapy (or any other form of follow-up treatment). The case for early adjuvant radiation clearly increases when the positive margin is larger; the Gleason pattern of the associated tissue is higher (4 or 5); and the patient’s PSA is rising significantly

  36. Hi Arthur,

    Which usually comes first when prostate cancer has spread: a fast, high-rising PSA or pain at the site where the cancer has spread?


    Arthur responded as follows:

    Dear Charles:

    Arthur says that, unfortunately there is no perfect answer to that question. It seems to vary from patient to patient, and it probably depends on the individual biology of the patient (the “host”) and the precise biology of the tumor (the “foreign body”).

    Arthur is aware of all of the following: (a) men who have been diagnosed with initial PSA values of > 20,000 ng/ml and widespread metastatic prostate cancer to bone but no evidence of actual bone pain at time of diagnosis; (b) men with have been diagnosed with PSA values of < 10 ng/ml, evident metastatic disease, and no bone pain; (c) men with PSA levels of 50-100 ng/ml, minimal metastatic disease but significant bone pain; etc.; etc. In other words, the possibilities are all over the map.

    Having said that, Arthur thinks it should be noted that (in general) in men getting diagnosed and treated in America today, the commonest signal of risk for metastatic disease is a PSA that is rising rapidly, i.e., men with a PSA doubling time of 6 months or less, but no sign of metastasis and no bone pain whatsoever. To that extent, in men at risk for potentially lethal forms of prostate cancer, a rapidly rising PSA does tend to occur prior to any indication of bone pain or metastatic disease. And a PSA that rises at that sort of rate would be extremely unusual in any patient with true Gleason 3 + 3 = 6 disease.

  37. Hi Arthur. I had corresponded with Dr Krongrad in September 2013 but since you have been answering questions directed to him for some time I thought I would contact you directly for an opinion.

    A brief history: PSA 8.69 July 2012 at age 63. Biopsy results were 3/21 cores positive, all three were Gleason (3 + 3) 6, stage T1c; negative bone scan and MRI. Brachytherapy was done in September 2012. PSA nadir of 2.21 reached 6 months post-op. A rising PSA at 9 months topped out at 7.6 in August 2013. MRI suggested metastasis to spinous process of L5 vertebrae. Urologist in South Africa recommended starting continuous ADT. Went to M. D. Anderson in Houston for a second opinion. They confirmed the metastasis with a needle biopsy of the lesion in L5. Their recommendation was a short course of ADT (6 months) followed by radiation to the L5 lesion, then cessation of the ADT while watching the PSA. I chose the latter approach, and returned to M. D. Anderson in March 2014 for 2 weeks of radiation therapy (12 fractions of 3 Gy each) After the 6 months of ADT my PSA was down to 0.20 ng/ml at the start of radiation therapy and a new CT scan showed a smaller lesion in L5 with sclerosis around the perimeter, which they said indicated new bone formation. Last week, at my first 2-month check of PSA and testosterone after the radiation therapy, my PSA was < 0.02 (undetectable?) and my serum testosterone was barely above castration level at 23. My oncologist at M. D. Anderson was hopeful that the L5 lesion was a solitary metastasis and the radiation oncologist there believed that the radiotherapy had eradicated what remained of the lesion. After 2 years of mostly bad news regarding my prostate cancer, I know it's too early to get too excited about this, and I will have PSA/testosterone tests every 2 months, but it does seem like very positive news. Dr Krongrad commented that the treatment plan at M. D. Anderson was somewhat unusual but thought it might be curative in intent. Are you familiar with others who have had similar treatment plans for metastatic prostate cancer? And secondly, would you attribute the drastic drop in PSA to the lingering effects of the short course of ADT or to the radiation therapy to the metastatic lesion? As an aside, I feel great and go to the gym 5 days a week for running and weight training. Enjoy your posts.


    Arthur responded as follows:

    Dear Allen:

    Arthur notes that the use of short courses of ADT in combination with “spot” radiotherapy for the treatment of men with apparently isolated areas of metastatic prostate cancer is not new, but it has started to become much more common in recent years. Why? Because it has become possible (with the development of new technology) to direct the radiation with much greater accuracy to isolated sites of metastasis, thus increasing the therapeutic benefit and reducing the risk for side effects of radiation therapy on surrounding tissues.

    While Arthur is not yet aware of any really sound, long-term data on the efficacy of this type of treatment in either eliminating metastasis or extending overall or prostate cancer-specific survival, there does seem to be a growing belief that this type of treatment is beneficial for carefully selected patients. Arthur hopes that someone, somewhere (e.g., at M. D. Anderson) is actually tracking long-term follow-up data on a large series of patients so that we can begin to get a clearer idea of the potential benefit of this type of treatment.

    Arthur is in no position to be able to tell you categorically whether your current PSA level can be attributed to the results of radiation therapy or to the lingering effects of the ADT. It may well, for example, be a combination of the two. This will probably become a little clearer over the next couple of PSA test results if you see your PSA re-stabilizing at a new level that might be closer to 1 or 2 ng/ml. Arthur would encourage you not to become too concerned if your PSA starts to rise a little over the next couple of PSA tests. Your serum testosterone level should also start to rise back to a normal level of 300 ng/dl or more now that you are off the ADT. Given that your serum T level was still only 23 ng/dl when you had your most recent set of tests, Arthur would have to say that there is certainly still a lingering effect of the ADT, and it may take a little while for this to wear off completely.

    The bottom line here is that Arthur thinks you should feel positive about what has happened to date, but that it may be another 6 months or so before you and your doctors will be able to make an initial, realistic determination about the success of this treatment strategy in your particular case.

  38. Many thanks Arthur. As usual, your response was concise and to the point. I appreciate that you dispense pertinent information in a timely manner. I’ve found that getting this kind of information from my doctors, both here in South Africa and at M. D. Anderson, can be considerably more difficult. I’m returning to M. D. Anderson in September for further evaluation and will let you know what they think.

  39. Dear Arthur, I am back with my questions to you.

    My husband, PSA 920 in March 2013. A mysterious case. Casodex, Lupron and 6 weeks of radiation. Presently his PSA has remained stable at below 0.05; he is only on Lupron.

    He seems to have an unusual reaction to the Lupron where — as happened in the first month after the first injection (starting 5 days after), he becomes ill, flu-like, very pale and weak, with GI issues and respiratory issues. It took us a while to see this pattern as we kept thinking it must be a virus, but now we know for sure it is the Lupron. We mentioned this to the oncologist and the nurse practitioner; they said it was unusual. Also, the month before he is due for his next injection, he feels “great” with no symptoms at all. We just switched from q4 months to q3 months. The side effects were less severe, but more shortness of breath for 2 weeks this time: very severe and he had to take off from work. He becomes a very strange, pale, almost grey color during these weeks on and off.

    After telling this all to the oncology department, they had said he is now considered as an “attempt to cure” (due to his PSA and no clinical symptoms) and may be able start intermittent therapy after he has completed 18 full months of Lupron therapy. It almost seems like he is metabolizing Lupron rapidly or unevenly. I suggested we repeat all scans and, if it looks like lymph nodes are shrinking and no evidence of bone involvement, we could try this. They agreed. Our next appointment is June. He is due for another Lupron injection, which he would receive. All his blood work is beyond excellent (like a 20-year-old’s); better than before the prostate cancer diagnosis, except that his liver enzymes are elevating. Do you think 18 months of Lupron may be enough? Most studies still say 2 to 3 years.

    Thank you again for your helpful input.



    Arthur responded as follows:

    Dear Susan:

    Arthur is glad to hear that your husband’s PSA is low and stable at around 0.05 ng/ml. That’s a very good response for someone who started out with a PSA of nearly 1,000 ng/ml.

    Re the odd, initial reactions to each shot of the Lupron, and the fact that he feels really well near to the end of the time period for each injection … It sounds to Arthur as though your husband is having some sort of unusual immunobiological reaction to Lupron therapy which dies away each time after his body adapts to the new injection stimulus. Arthur really doesn’t have any particularly bright ideas about how one might try dealing with this. One possibility would be to ask about trying a different LHRH receptor agonist (such as goserelin acetate/Zoladex or triptorelin pamoate/Trelstar instead of leuprolide acetate/Lupron). This is something you’d need to bring up with the doctors and see what they think. Your husband’s reactions to the Lupron are certainly unusual, and you and the doctors do need to be monitoring this with care.

    With regard to the idea of switching your husband to intermittent ADT … Arthur can certainly see the argument in favor of doing this, particularly given the benefits of being able to cut down on the number of injections (with the odd set of side effects). Having said that, Arthur would be concerned about whether switching to intermittent ADT is an appropriate strategy for any man who had started out with a PSA level of 920 ng/ml after just 18 months. Could it be tried? It surely could! Is your husband likely to be able to maintain a low PSA level for more than about 6 months off the ADT? That’s a much harder question to answer!

    Some other things you might want to discuss with the doctors if you want to try the intermittent ADT approach are: (a) having your husband take a drug like dutasteride/Avodart alone while he is off the ADT (on the grounds that dutasteride will continue to block the conversion of testosterone to dihydrotestosterone during the “off ADT” period); (b) asking the doctors to monitor your husband’s serum testosterone and serum dihydrotestosterone levels during the “off DHT” period (as well as his PSA levels) to see how fast these are rising.

    The goal in all of this is not just to try to control your husband’s PSA level and keep it low and stable. The real goal is to extend his life for as long as possible while ensuring a good quality of that life. That is going to require a very careful balance intended to limit the use of Lupron (and perhaps other drugs) to the minimal amount needed to effectively delay progression.

  40. Dear Arthur:

    Thank you again for your excellent advice. It is true no one seems to know how long is too long with ADT and what time line would be too short. I was told another study may be released in June regarding the 18-month approach and how successful it was.

    I was also thinking possibly monthly injections? For the next 3 to 9 months whatever decision is made?Lupron seems to work so well and quickly for him as his T level is so low, below 20 and was that low after first injection. We get it checked every 2 to 3 months. I had asked to have his DHT done, and was told that with his T level so low he could not produce much DHT. Is this correct? I will question it again. I also know how blessed he is with his excellent response and am concerned with the 18 months (as no one really knows), but would like his quality of life to be better. As I had mentioned before, we also use alternative medical methods, supplements, and foods and will continue these. I am glad the new studies on vitamin D have been released. My husband had a vitamin D level of 11 at diagnosis. The study revealed that < 12 was associated with the most aggressive cancer. Who knew? I kept asking every doctor about it, no one seemed to connect his extremely low level of vitamin D to the prostate cancer. I pumped him up to 50 last year after reading older studies on vitamin D and prostate cancer. He does seem to be having an unusual path from diagnosis to response to side effects with this illness.

    Thank you for your time and knowledge.



    Arthur responded as follows:

    Dear Susan:

    You need to understand that, with regard to vitamin D, there are all sorts of good reasons why a man with low vitamin D levels like you husband may need vitamin D supplementation. However, whether your husband’s prostate cancer was either caused by or is being in any way driven by his vitamin D levels is much more difficult to ascertain. The new vitamin D data are still based on epidemiological “association” studies. Such studies are hypothesis-generating but they do not offer clear data about causes and effects for specific disease and their outcomes. People can all too often over-react tho these types of epidemiological data, and they are often shown to be misleading … so just be a little cautious about over-interpretation.

    With respect to the DHT levels … Yes, in theory, if a patient’s serum T level is very low then he should have an extremely low DHT level. However, if your husband is going to come off the ADT, then the reason Arthur thinks it would be wise to assay his DHT level now is because his DHT will start to rise again, as will his serum T level. It might be wise to know the current baseline and then monitor the rise in his DHT level.

  41. Thank You , Yes a baseline DHT would be good. Susan

  42. Dear Arthur,

    Again I have to seek your advice. My husband just received his PSA after 15 months on Lupron. After being below 0.05 for almost 10 months his PSA was 0.08 this week. We were told it is not of concern and to have it repeated in a month instead of 3 months. His liver enzymes are also elevated. These are to be repeated again in a month also. Our oncologist suspects his metformin may be causing this. We switched to monthly injections of Lupron this week to see if his side effects would be less. His testosterone level had been below 20 but have not received results yet from this blood draw. Is there anything else we should be doing in this month’s time? Is this increase of concern? He has no prostate clinical symptoms, but never really did. We are scheduled to see his internist in 3 weeks to follow up on the liver enzymes.

    Thank you for your time.



    Arthur responded as follows:

    Dear Susan:

    It sounds to Arthur as though you are already doing everything you should be doing. Arthur says that this is really a very, very small change in PSA level, and getting a repeat PSA in a month and then checking on the liver enzymes seems entirely appropriate. Hopefully your husband’s PSA will either drop back down to 0.05 or simply restabilize at 0.08. Of course if the PSA were to keep on rising then that will be a different story.

  43. Thank you again; good advice as usual; it will be a long month. All other blood work is textbook perfect. Testosterone below 3. The monthly Lupron shot is a whole different world so far. He has had none of the crazy side effects, just the documented common ones. Hope you are well.


  44. Hi Arthur. A follow up to my post to you on May 14, 2014. I had my second 2-month check of PSA/testosterone post-radiation therapy at M. D. Anderson in March. As you predicted the PSA rose from undetectable 2 months ago to 0.13. The shocker was the total testosterone rose from 23 ng/dL to 674.35 ng/dL. The effects of the 6 months of ADT have really let go and there are no more hot flashes and sexual function has returned to the good level I had before beginning the ADT. I’m returning to MD Anderson in September for new bone and CT scans. Would you expect PSA to rise even more due to the higher testosterone? Any rise is worrisome but I still feel pretty positive.

    Thanks, Allen



    Hello Allen.

    Arthur thinks that the rise in your PSA to 0.13 ng/ml is reasonable under the circumstances and the rise in the serum T level is obviously near to ideal. The key question is probably going to be what your next PSA test results shows. Arthur would strongly suggest that you get a next PSA test result in South Africa (where you presumably got the most recent test done) before you go back to M. D. Anderson, so that you know you are comparing apples to apples (as opposed to apples to oranges). M. D. Anderson will certainly want to do their own PSA test, but you need to know that you can accurately compare your most recent test result to a follow-up test done at the same South African lab.

    If your next PSA result in 2 months time was to come back at 0.25 ng/ml or thereabouts, then Arthur would have a concern that your PSA was rising fast (i.e., doubling every 2 months) and that, consequently, the treatment given by M. D. Anderson had not had the fully desired effect of putting you into a long-term remission. However, if your next PSA results was to come back in the (say) 0.10 to 0.17 ng/ml range, then this would suggest that a long-term remission was a real possibility.

    The fact that your serum T has returned to truly normal levels is a good thing. That’s where you want it to be if you are truly in remission. If you are not truly in remission, then it will only be a matter of time before you have to be back on the ADT, and you’ll have to cross that bridge when you get to it (if you do).

  45. Many thanks Arthur. I’ll take your advice and have a new PSA done here in SA before I travel to Houston in September. Allen

  46. DRE clear; bone scan clear; PSA > 10 for many years, rising slowly to 24 ng/ml now. Why isn’t a 3 T MRI used to determine the location and extent of the tumor? I have had two random 12-core biopsies about a year apart. The first one showed a small amount in one core, with a Gleason score of 3 + 3. The latest one again showed a small amount of cancer in one core, with a Gleason score of 4 + 4. I’ve asked for a multi-parametric 3 T MRI to define whether or not the tumor is singular or not and if another biopsy is requested could the data be used to define the location of the cores. My HMO has refused this as not being a current standard practice. Yet I read that a large number of places are doing it. Is this an unreasonable request?

    I am 80, in very good health (some family members are into their 100+ years) and think that the more information I can gather now may be helpful in the future. The HMO want to do Lupron and then IMRT and are telling me that waiting much longer will be dangerous. What do you think?



    Arthur responded as follows:

    Dear Allen:

    Clearly Arthur is missing a lot of information here, so it is a little difficult for him to address with accuracy all of the issues you raise. However, here are some of the key factors that may be relevant:

    — The exact nature of your insurance coverage and the HMO that you belong to.
    — Whether there is any provider within your HMO’s network that can actually give you an appropriate multi-parametric MRI (let alone a 3 T MRI).
    — The fact that until your most recent re-biopsy, you appeared to have low-risk prostate cancer that (arguably) could simply be monitored.
    — Whether you had been offered treatment earlier.
    — The use of MRI-guided biopsy for localized prostate cancer is not yet considered to be standard practice by anyone. Indeed, it is arguably only within the past 18 months that sufficient data have been published to start considering whether this type of biopsy should become standard practice in the future.

    Most of the people who have been getting 3 T MRIs to date have been paying for them out of their own pockets (unless they were getting them as part of a research protocol at somewhere like the NCI’s Clinical Center in Bethesda, MD).

    Arthur would politely but strongly suggest to you that you need to separate your irritation with your insurance provider about your belief that you should have the 3 T MRI from the fact that you have now been shown to have high-risk prostate cancer with a PSA level of 24 ng/ml and a Gleason 4 + 4 = 8. This is potentially highly aggressive form of prostate cancer and could kill you if you don’t get it treated.

    Arthur would advise you that surgery for prostate cancer in an 80-year-old would very, very rarely be wise. The recommendation of a short course of an LHRH agonist like Lupron (for say 3 to 6 months) in association with radiation therapy is, on the other hand, an entirely appropriate form of treatment under the circumstances. And the result of a 3 T MRI test is most unlikely to change that recommendation at this point in time.

    Arthur understands your belief that “the more information [you] can gather now may be helpful in the future”. However, there comes a point at which action may be more important that information. A good radiation oncologist is almost certainly going to want to give you a CT scan or an MRI as part of the radiation treatment planning process, and so this may help you to garner information. It is also relevant that lots of very smart radiologists and prostate cancer specialists are of the opinion that a well-conducted multi-parametric 1.5 T MRI can provide almost exactly the same amount of information as a 3 T MRI anyway (given a skilled uroradiologist who knows how to read such scans).

    Arthur thinks that you do need to get treatment and that you do need to get it soon, given your current situation. While being able to have a 3 T MRI as part of the planning process might well be “ideal”, waiting for the “ideal” to happen may be placing your life at risk.

  47. Thanks. I am 44, white, and heathy; parents are 60 and healthy. I will see another urologist since the group I saw seemed to be all about billing for procedures (walk in the door — urine sample, bladder ultrasound every visit). Also tried to sell me on cystoscopy for BPH, MRI, biopsy, etc.

  48. Hi Arthur. I am 67 and have prostate cancer. My Gleason score is 6 (3 + 3); my clinical stage is T1cN0M0; my PSA went from 1.2 to 1.95; my dad and three uncles on my mother’s side had prostate cancer; my DRE is normal. I live in southern New Hampshire. Where or how do I find a list of skillful urologic oncologists who specialize in da Vinci prostatectomy?


    Arthur responded as follows:

    Dear Paul:

    Arthur says that he is not aware of any good “list of skillful urologic oncologists who specialize in da Vinci prostatectomy.” However, because you live in southern New Hampshire there are quite certainly a number of highly regarded prostate cancer treatment centers within a couple of hours drive at places like Massachusetts General Hospital in Boston and the Lahey Clinic in Burlington, Mass. In addition, you could contact one of the Us TOO Support group leaders in New Hampshire or Massachusetts and ask them if they are able to give you specific recommendations. To find these support group leaders names and contact information, just click here and then look at the listings for New Hampshire and Massachusetts. A third way to find such a urologic oncologist is simply to ask the urologist who diagnosed you who he would go to if he wanted to have da Vinci surgery. Most good urologists are very willing to make such referrals for a second opinion.

    Arthur would also point out that one of the other things that you should really discuss with a good urologic oncologist, however, is whether you have a form of low-risk prostate cancer that can simply be monitored (on active surveillance) as opposed to needing immediate treatment. You haven’t given Arthur all of the relevant information that would help to determine whether you would be a good candidate for active surveillance, but you do appear to have either low-risk or very low-risk disease. The fact that you had several relatives who were treated for prostate cancer doesn’t necessarily imply, on its own, that you have clinically significant disease. Far too many cases of low-risk prostate cancer get over-treated when they could simply be monitored because they don’t actually need invasive treatment.

  49. Thank you, Arthur.

  50. I agree with Arthur that you may not need any treatment yet. I am close to you and am on active surveilance, now and hopefully a long time.

  51. Hi Arthur!

    Since April 2013 (after surgery in August 2012) my PSA has risen from 0.028 to 0.047 using the ultrasensitive PSA test (same lab) given every 2-3 months. There have been fluctuations at times — an example of that is the last three test results, which were 0.044, 0.042 and the latest 0.047. I am 2 years post-surgery.

    I know that using the standard PSA test (< 0.1) would have me still in the undetectable range but what could possibly be going on with my PSA at such a low level? Should I be overly concerned?


    Arthur responded as follows:

    Dear Mike:

    Arthur says that he would not be overly concerned about such a small rise in your PSA level at this stage — although you certainly need to keep a close eye on it.

    It is always very hard to know what might cause such very small rises in PSA level a couple of years after surgery. However, one possibility might be that there was a very small amount of non-cancerous prostate tissue (perhaps near the prostate apex) that your surgeon was unable to remove at the time of your surgery. Such a tiny piece of tissue can sometimes enlarge over time, producing very low amounts of PSA which then might account for this small rise in your PSA level.

    Your should really discuss this with your urologist and come to a decision with him (or her) about what you would both want to do about this if your PSA was to start to get up closer to something like 0.07 ng/ml and depending on the speed at which your PSA was increasing at that time. In other words, be ready in advance to take action at a predetermined PSA level so that everyone knows what they are going to want to do if action does seem to be appropriate.

  52. Hi Arthur!

    I went over my post-RP pathology report and the only two “negatives” found were my final Gleason total was 7 (3 + 4) and a small positive margin at the apex with a Gleason grade of 3 at that margin. Could this be the guilty culprit causing the minor increases and decreases in my PSA level? If so, would it be wise to start salvage radiation right away or will waiting until recurrence (0.2 ng/ml) is evident be sufficient? I ask this because I’ve heard that not all positive margins will cause recurrence. Also some men have reached 0.1 ng/ml and never progress any further!


    Arthur responded as follows:

    Dear Mike:

    Arthur says that, first, yes, your small rise in your PSA level could be in some way associated with the positive surgical margin; second, no, Arthur does not believe you need to be rushing off to a radiation therapy suite yet. As you have noted, there are men who do indeed have this type of small rise in their PSA post surgery and then the PSA can stabilize again.

    As Arthur said previously, you do need to keep a careful eye on your PSA, but (subject to anything that your urologist is telling you otherwise) Arthur thinks you can afford to limit your immediate management of the situation to just monitoring that PSA level.

  53. I read with interest your response to Mike because I too have questions about the practical usefulness of the ultrasensitive PSA test. I am a relatively healthy 67-year-old who had a prostatectomy 17 months ago. My pathology report indicated: (a) a Gleason score of 3 + 4 = 7 with tertiary pattern 5 and the tumour involving 5% of the gland; (b) pathologic stage pT3a with focal extracapsular extension and no regional lymph node metastasis; (c) negative margins, but many areas with the tumour < 1 mm from the margins; and (d) lymph-vascular and perineural invasion. Urinary and sexual side effects are relatively modest and manageable. I have had six post-surgery PSA tests with continuously increasing values: 0.009, 0.011, 0.012, 0.020, 0.026, and 0.032. Does this slow but steady increase in PSA give me early evidence that cancer has recurred and that it would be to my advantage to risk more side effects and begin salvage radiation now? Or are these PSA results of little practical value and I would have the same outcome without risking earlier side effects if I waited until my PSA reached the old 0.2 standard for recurrence? Is there any evidence or expert opinion that might inform my decision?


    Arthur responded as follows:

    Dear Ray:

    Arthur says that without knowing the precise dates of each of your post-surgical PSA tests, and given the inherent difficulty of establishing accurate PSA doubling times for men whose PSA values are all < 0.1 ng/ml, it is hard to know exactly what your PSA doubling time might be. However, if Arthur assumes that these six PSA tests have all been taken at roughly 3-monthly intervals and processed at the same laboratory, then it appears that your PSA doubling time is of the order of 9 months or so. However, Arthur suggests that you can't read too much into this because all your PSA values are extremely low and so minor inaccuracies in any of the levels might substantially affect the overall estimate of PSA doubling time.

    Arthur's entirely personal opinion is that unless your PSA level was to make some sort of sudden jump (say to 0.070 ng/ml or thereabouts when you got your next test results) there is no good reason to be rushing to the radiation oncology suite as yet. Indeed, Arthur would argue that these data are of considerable value in helping you to appreciate that you don’t need to take that type of action as yet, even though your pathological data post-surgery do indicate that you are at a higher risk level than anyone might have wanted to see (most particularly because of the tertiary Gleason grade of 5).

    Quite why your PSA is rising is obviously impossible to determine with any level of certainty when it is this low, and Arthur assumes that you have already had this conversation with your doctors, who have also not been recommending salvage treatment as yet.

    Arthur cannot tell you with any level of certainty that you will or will not have a formal biochemical recurrence (defined by a PSA level of 0.2 ng/ml or higher), let alone a real clinical recurrence. If your PSA was to go on rising at the current rate, then you would probably hit a PSA of 0.2 ng/ml in something like 2 years time, and you would know within about 18 months that that risk was imminent. In Arthur’s view, that would probably be a good time to re-assess what you want to do.

  54. Arthur,

    It is very rare that I disagree with your analysis and recommendations, and my disagreement here is fairly minor.

    First: If the six data points occurred at regular time intervals, I calculate a PSA doubling time of about 2.65 to 2.80 times the interval between tests. If the tests occurred every 3 months, this translates to a PSADT of 247 days — closer to 8 months than 9 months, with formal biochemical recurrence (PSA ≥ 0.2) occurring roughly 650 days after the date of the “PSA = 0.032” result.

    Secondly: The data points fit a curve of exponential growth remarkably well (chi-squared = 0.1 for hypothesis “PSADT = 247 days”). If there were only three or four points, or if the fit were poorer, there would be far less confidence that the calculated PSADT was a good metric.

    Because of this, I disagree with what you say about “a sudden jump to 0.070”. The six data points so far provide no reason to expect any sudden jump, and every reason to expect PSA = 0.070 to be reached through normal exponential growth about 9 months after the “PSA = 0.032” result (if testing occurs every 3 months).

    Therefore, I think this gentleman’s case presents a very good reason for reconsidering the arbitrary “PSA = 0.200” cutoff point. His data are superbly precise — vastly better than the data supporting the traditional guess.

    If I were in his shoes (and, actually, mine are fairly similar with a remarkably consistent PSADT of 61 days when I’m not androgen-suppressed), I would look for another two or three data points over the next 6 to 9 months and, if the regular clockwork doubling continues, to consider taking action at that time.

    The usual caveats apply:

    • If the PSA testing was conducted at regular intervals other than 3 months, then the analysis stands, but the timescale should be adjusted.
    • If the PSA testing occurred at more irregular intervals (aside from the “0.012” value possibly being measured early), then the analysis is suspect, and action should be deferred until the data are better.
    • As always, one must consider the tradeoff between quality-of-life vs postponed-onset-of-symptoms. If the gentleman is 90 years old or in poor health, then it makes no sense whatsoever to consider a measure with considerable side effects that might, if successful, merely gain a postponement of onset-of-symptoms (e.g., at PSA = 200) from an estimated 8 years hence to an estimated 15 to 20 years hence.


    Arthur responded as follows:

    Dear Paul:

    Arthur thanks you for your observations.

    Arthur would just like you to note that your observations do not actually disagree with Arthur’s prior comments, for a couple of reasons.

    In the first place, Arthur was being very careful not to specify a precise PSA doubling time for this gentleman, based on the available data. Arthur wrote that “it appears that your PSA doubling time is of the order of 9 months”, which is not the same as saying that it is 9 months. This was a very deliberate statement, because there are almost no validation data on the use of PSA levels less than 0.1 ng/ml to assess PSA doubling times, and we have no precise dates for the gentleman’s tests.

    Second, Arthur wrote that “unless your PSA level was to make some sort of sudden jump (say to 0.070 ng/ml or thereabouts when you got your next test results)”. Does Arthur think this is probable in this particular case? No, he doesn’t, but these things do happen, and if there was to be such a sudden jump in the patient’s PSA level, this would (potentially) be indicative of a sudden acceleration in the patient’s PSADT and (for whatever reason) a change in his risk level.

    Finally, we do know this patient’s age. He states that he is 67.

    Please understand that Arthur does not disagree with your observations. Arthur would only note that he was very carefully trying to avoid the level of accuracy of interpretation that you are suggesting, precisely because of all the caveats that you list at the end of your comments, many of which Arthur also stated or implied in his comments.

    Arthur feels that the important thing, above all, for this patient is that he continues to monitor his PSA level, just as he has been, under the supervision of this doctors, and that he understands that the currently available data do not necessarily suggest immediate intervention. Precisely when any future intervention might be recommended is going to depend on actual future data (as opposed to speculation about what those data might be or when they might suggest intervention — if they ever do).

  55. Hi Arthur. A follow up to my post on July 14.

    I took your advice and had a PSA done here in South Africa 5 days before I was seen at M. D. Anderson. The test here showed an increase from 0.13 to 0.32 — a little discouraging. However, just 5 days later the lab at M. D. Anderson had the PSA at 0.20 which is the level it was at 6 months ago when I had the 12 fractions of radiation to the spot of metastasis to bone in L5. My oncologist at M. D. Anderson said that since I still have a prostate gland (treated with brachytherapy 2 years ago) I am allowed to have some level of PSA present. Since I have been off of the ADT and radiation for 6 months with a stable PSA he thinks I am in a remission that could last a year or 5 or 10. New bone and CT scans showed nothing new and healing of bone where the spot was on L5. I am currently under no treatment what so ever and am only to have quarterly PSA tests and only have to have another 6 months of ADT if the PSA reaches 1.0. I have never heard of active surveillance on a patient who has had brachytherapy, then metastasis to bone, then ADT and radiation therapy, but I think that is where I am at. I was told that I don’t need to return for new scans for the foreseeable future. I’m pretty happy with the results of my latest visit back to the States. Allen S.


    Arthur responded:

    Dear Allen:

    Arthur doesn’t consider “active surveillance” to be the most appropriate term for the type of monitoring that is recommended for someone who has had treatment and appears to be in at least potentially long-term remission (even though it has started to be used). As far as Arthur is concerned, the important thing is that you appear to be in remission; that remission could indeed last for years; and anyone in this type of remission needs regular tests to make sure that they are remaining in remission.

    As discussed with your oncologist (and as indicated by the slight differences between your PSA in South Africa and your PSA at MDA) you do need to be careful to ensure that you don’t over-react to small variations in your PSA level like this. If you see such an event, your first question for your doctors should probably be, “Do you think we need to get a repeat PSA level in a month to check this out?” rather than to assume there is a problem. Arthur says that least you now have a baseline from the lab in South Africa to work from in addition to the data from MDA.

    Hopefully your PSA will stay down at this sort of level for the next 20+ years!

  56. Hello Arthur, it is Susan again.

    My husband’s PSA stayed at 0.08 and is now down to below 0.05 again — a little bit of a bounce, due to radiation? Unsure. Has been 13 months since completed.

    All has been well and he feels great since receiving the monthly Lupron injections rather than the 3- or 4-month preparations. Unfortunately his liver enzymes (AST and ALT) continue to rise. Our internist and oncologist are stumped. They ran tests for hepatitis (not back yet). I also noticed that his triglycerides have been rising rapidly (no one mentioned them). His cholesterol is low: below 150, good ratio. The oncologist ordered abdominal and pelvic scans and a bone scan is set for next week. She is not saying the cancer is spreading but wants to be sure. I did some research on my own and found non-alcholic fatty liver disease. His lab values seem to fit this diagnosis perfectly. He has not gained any weight in the past 2 years, but I thought it may be related to the past Casodex or present Lupron. Have you heard of this? I guess we will know from the scans. He eats a relatively low fat diet.

    Thank you.



    Arthur responded as follows:

    Dear Susan:

    Arthur says that it is really quite impossible for him to give you any meaningful advice about why your husband’s AST/ALT and triglyceride levels have been rising. It is true that this would occur in a man with non-alcoholic fatty liver disorders, but these liver enzyme levels could be rising for all sorts of other metabolism-related issues too.

    All that Arthur can really tell you under the circumstances is that you and your husband are going to need to work with your doctors to try to identify what the problem is. It could be related in some way to the Lupron treatment; it seems unlikely to be associated with the Casodex, since this has been stopped. And if your husband is on a low-fat diet, and doesn’t drink, it makes no sense that he would have fatty liver disease. (Arthur says, are you sure he isn’t sneaking out to the bar twice a day for a couple of shots!? )

  57. Does hormone therapy given 3 to 6 months before radiotherapy, during radiotherapy, and for 2 to 3 years after really destroy occult metastases?


    Arthur responded as follows:

    Dear George:

    Arthur says that it is clear that androgen deprivation therapy (ADT) can reduce the size of both evident and occult metastatic prostate cancer lesions. Whether it can actually eliminate them entirely on its own is less clear.

    The way Arthur thinks about this is that if one is able to limit the growth of occult metastases (in the lymph nodes and other tissues in the pelvis) among men with locally advanced prostate cancer, one increases the ability of other modalities (most particularly radiation therapy and the patient’s own immune system) to actually eliminate the remaining cancerous tissues.

    An analogy might be the way we use relatively mild weed-killing agents to treat the weeds between the cracks in our patios or driveway. These weedkillers don’t actually kill all of the weeds, but they reduce the overall size of the problem, making it easier to them eliminate the odd ones that remain (by simple weeding or more intensive forms of “treatment”).

  58. Dear Arthur,

    Ha, I am sure, he has a very mentally demanding job and no availability to do that. Cheesecake maybe! But I doubt it. He has been losing weight or has been stable for the past 4 years. Besides the ALT and AST ratio indicate non-alcoholic liver disease. He does drink socially on weekends but never more than two drinks a day. I guess we will have to wait for the scans. I thought maybe the Lupron raised his trigylcerides, although I can find little to document this. But I could find little to document his strange reaction to the Lupron 3- and 4-month preparations and how deathly ill he was after each shot for weeks. The oncologist feels it may have been a reaction to the extended release preparation that is used.

    Thank you



    Arthur responded:

    Dear Susan:

    Arthur says that he is sorry that he can’t offer any more insight about all of this. The oncologist may well be correct that your husband was having some type of allergic reaction to whatever is used to create the 3- and 4-month extended release formulations of Lupron.

  59. Arthur,

    I am a 66-year-old white male, on no meds and healthy. I have been getting PSAs and DREs for at least 17 years. My PSAs have been low from 1998 to 2010. Since then they have been: 2010 PSA = 2.1, 2011 = 2.8, March 2012 = 3.4, May 2012 = 2.7, June 2013 = 3.0, June 2014 = 3.4, Oct 2014 = 3.9.

    Now, I have been told by a urologist friend that the thinking on PSA levels have changed a little and as you grow older PSAs can rise and the magical number of “4” is no longer as critical as it once was.

    Should I be concerned about my PSA going from 3.0 to 3.9 in 15 months? Should I now have a PSA every 3 months to see where it goes from here? I know that the big jumps are of most concern. Would it be wise to have a biopsy? … I have always been very proactive regarding my health.

    Thank you,



    Arthur responded as follows:

    Dear Joe:

    Arthur would first like to confirm for you that the “magical” number of “4” has been known for some considerable time to be a lot less “magical” than it seemed to be back in the late 1980s and early 1990s. Your urologist friend is completely correct about that.

    Second, the important question that you need to get clear is whether there may be other good reasons why your PSA level has been rising. For example, does your primary care physician think that your prostate feels larger than it did a few years ago? Have you been having slightly more problems with urination (a slower stream, more difficulty fully emptying your bladder)? Things like this could indicate that your problem is more likely to be the very common benign prostatic hyperplasia (BPH) than prostate cancer.

    Third, Arthur would point out that a test called a free PSA test (which can be carried out in conjunction with your next standard or “total” PSA test) can help to discriminate between risk for prostate cancer and risk for BPH. Low “free” PSA levels (below 10%) are more likely to be associated with risk for prostate cancer; higher “free” PSA levels are more likely to be associated with risk for BPH. And BPH is a very common and near to “normal” condition among aging men.

    Finally, Arthur would note that if you and your primary care doctor do decide that a referral to a urologist and biopsy is a good idea, for any reason, Arthur would recommend that, if at all possible, you try to have such a biopsy done after a multiparametric MRI that allows for targeted biopsying of any suspicious areas of the prostate. While it is always possible that you have a small amount of prostate cancer, at 66 years of age you actually want to avoid treatment for low-risk prostate cancer of any type for as long as you can in order to optimize your quality of life. At 66 years of age, a low-risk form of prostate cancer would be highly unlikely to be the cause of your demise.

  60. Arthur,

    Thank you for your response. I do have BPH and last year had a CT scan after urologists in Florida scared me (and probably other seniors after a free screening) and the scan showed my prostate to be 4.8 x 5.5 x 5.7 cm with calculated volume of 79 cc. No focal mass or abnormal enhancement, etc., etc. My prostate is very large but my quality of life is fine. I have been taking saw palmetto and pumpkin seed oil. I get up generally once at night.

    Also, my Dad is 91 and has no problems at all with anything! And he only gets up once a night (and could put out a fire!). Mom is 90 in good health!

    Last year I had a small mass (16 x 13 x 13 mm) ablated from my right kidney and will see the urologist surgeon/oncolologist who did it for a 1-year follow-up so I will bounce what he says about my PSA with what my personal urologist (friend) says. I always get several opinions, always! Like you said and what I have read … men are getting too much treatment that they really don’t need!

    Part of my problem is, I worked in the pharmaceutical business and my team marketed prostate cancer medications so I know too much but anxiety tends to clouds my thinking?

    Thank you so much for your input!



    Arthur responded as follows:

    Hi Joe.

    Arthur says that sounds like a potential plan.

  61. Hi Arthur!

    Does every man eventually progress to metastatic prostate cancer once his cancer has recurred (PSA 0.2 and rising) if he doesn’t get any secondary treatment?


    Arthur responded as follows:

    Dear Mike:

    Arthur says, “No.”

    Many men will die of something else long before their cancer metastasizes or at least long before metastasis is either evident or causes symptoms. The key issues that need to be considered are the speed at which the cancer is spreading (which can be estimated through the use of a PSA doubling time calculator) and the inherent risk for an individual patient based on things like his age, his life expectancy, other co-morbid conditions, his original PSA level at diagnosis, his Gleason score on biopsy or (better) after surgery, and his clinical or pathological stage.

    Arthur would emphasize that risk of metastasis can only be assessed individually for each patient, and he believes that any really skilled and experienced clinician who understands the natural history of prostate cancer would tell you the same thing.

  62. Hi Arthur. Is it possible to accurately calculate PSA doubling time with an ultrasensitive assay at very low PSA levels? For example, my PSA level was at 0.028 in April 2013 and went to 0.055 in October 2014 with tests given every 2-3 months apart. Given that information, is it 18 months? Or is the standard assay more reliable at calculating PSA doubling time?


    Arthur responded as follows:

    Dear Mike:

    Arthur says that the accuracy of PSA doubling time based on very low PSA levels needs to be treated with a degree of caution. Most PSA doubling time calculators were developed based on data related to PSA values greater than 0.1 ng/ml. It is not a matter of the type of PSA test being used (ultrasensitive or standard) but more about the size of the variation in the test result over time.

    Having said that, Arthur thinks that if your PSA has gone from 0.028 in April 2013 to 0.055 ng/ml in October 2014 over a period of 18 months, with a slow but steady rise that has been reflected in a series of something like 5 to 7 PSA tests, then Arthur would certainly think that this is highly suggestive of a PSA doubling time of about 18 months.

  63. Hi Arthur. With the slow but steady rise and doubling time of 18 months, would salvage radiation at this point be considered over-treatment, not knowing if I would ever reach BCR (0.2 and rising ) or will monitoring every 2-3 months be appropriate at this point? The only negatives from my pathology report (based on a radical prostatectomy in August 2012) were a positive margin at the apex (Gleason 3 at margin) along with a final Gleason score of 3 + 4, and I’m young age 44 right now!


    Arthur responded as follows:

    Dear Mike:

    Arthur says that the appropriateness of early adjuvant/salvage radiation therapy in cases like this is highly controversial, with different physicians having different views of the situation. You really need to discuss this in detail with your doctors.

    There are arguments in favor of immediate radiation in cases like this … and there are arguments against this too. A great deal depends on your own personal opinions about the risks related to disease progression, to further treatment, and to the potential impact of further treatment on your quality of life … and whatever Arthur may think is really rather irrelevant to this because it is what you think that is going to be important. What you think may also depend on the degree to which you have recovered good erectile and sexual function post-surgery and the importance of your sex life. It’s obviously all going to be of some relevance to “Mrs. Mike” too (if there is a Mrs. Mike).

  64. Mike,

    I am 54 years old. I had radiation 3 months after RP, because my surgeon and oncologist told me that 3 months is the limit for adjuvant radiation to have any real benefit. After that, it may spread (if it exists), if it hasn’t already. By this point it was clear to me that I probably wasn’t going to regain any substantial erectile function (I know, it can take 18 months, but I had made no real progress after the removal of one nerve bundle) … and plus, with a positive margin and a PSA of 25, and Gleason of 3 + 4, I was a bit worried about the cancer returning. Even with adjuvant radiation therapy, I stand a reasonable risk. .. It’s been 2 years and I am almost due for a PSA check after 6 months. (My first one with that much of a time gap … previously every 3 months). So far they have been undetectable. I wrote because you need to be aware that the radiation will kill the nerves involved with erectile function … according to my oncologist over a period of 18 months to 2 years. If you have regained any function, as Arthur said, it may be downhill after the salvage radiation. In addition, there is damage to the bladder … irritation, incontinence. I was lucky … I recovered and am dry, but still have to urinate often at night. The irritation clears up relatively fast, over about 3-6 months. For me, I felt I had little to lose, and eventually went with an implant, but as stated, just be aware of the side effects.

  65. Hi Arthur!

    Had some questions and would like to get your expert opinion on the article from this website titled “When should the patient and doctor consider salvage radiation therapy.”

    Does this suggest that every man (with or without an adverse pathology report) with a PSA above 0.03 after RP proceed with salvage radiation because the stats show he will eventually experience BCR (> 0.2)? If so, then in your opinion why continue to use the standard assay < 0.1 (as undetectable) to monitor patients after RP? I'm confused! With the inconsistent results coming from ultrasensitive assays this would definitely put many men in danger of being over-treated when we know not all men with or without adverse findings on their pathology reports will eventually experience BCR. Example: my PSA 4 months ago was 0.055; the latest result from December was 0.04! Your thoughts please!


    Arthur responded as follows:

    Dear Mike:

    It is Arthur’s opinion that the only really concrete thing that we can take away from the data published by Kang et al. and Vesely et al. (and referred to in the above-mentioned article) is that there are very few men who really need to have immediate adjuvant RT: perhaps those with at least three pathological risk factors.

    For some time, it has also been Arthur’s opinion that any man with adverse pathology post-surgery would also be wise to request that his PSA levels post-surgery be monitored with care using an ultrasensitive PSA test. Why? Because it helps to assess risk for progression earlier than the standard PSA test. However, in Arthur’s estimation there is a big difference between assessing and understanding risk and taking action. Your own case is an excellent example of this.

    If Arthur had aggressive pathology post-surgery, he would, at this time: (a) want to have his PSA monitored using an ultrasensitive PSA test; want to see at least two or more successive increases in his PSA level to > 0.05 ng/ml or higher before he would even think about taking any form of action as salvage (radiation or otherwise); (c) even then, be very cautious about exactly when any form of salvage therapy should actually be implemented. We really don’t have any sound information about when is “best” to implement salvage radiation therapy that includes things like breakdowns by age and risk factors. Arthur is, perhaps, overly cautious about risk for over-treatment becuase he believes in “Better the Devil you know …”. However, for those men who are really terrified of living with a rising PSA, for whatever period of time, because they seriously believe that a rising PSA is a future, prostate cancer-specific death sentence, then knowledge of risk and implementation of early salvage therapy may well be a right and proper strategy.

    You seem to have been doing “what works for you”, and that is all that anyone can really do based on the currently available data. The implication (for Arthur) is that physicians need to talk to their patients not about “absolutes” but about options. And it is certainly an arguable option that any patient who receives whole gland surgery for prostate cancer today should have his PSA monitored post-surgery using an ultrasensitive PSA test. What he does (and when) if his PSA starts to rise based on such a test remains complex. “First do no harm” that could lead to over-treatment, in Arthur’s very humble opinion, remains a very important contextual factor.

  66. In general, are men more volatile after prostate surgery? My brother has always been gentle and calm? Twelve months later, he is angry and very cruel and sarcastic to even his customers. How can we help him. We want our “Jim” back. Thank you.


    Arthur responded as follows:

    Dear Penny:

    Arthur says that the psychological effects on many men of treatment for prostate cancer can be very problematic. Everything about the way men think and function is closely tied to their sense of masculinity and sexual function. Loss of that normal sense of masculinity and sexual function affects individual men in different ways — but social withdrawal and anger are not uncommon, and it can take patients a while to adapt. Sometimes that need to adapt is very, very hard for a man to accept.

    It sounds to Arthur as though your brother may need some professional help … but he may not even be willing to recognize and accept that. Obviously Arthur is missing a lot of information here. However, there are two pieces of material you may want to read to help you help your brother, and they may be helpful for your brother too:

    An article by Anne Katz, who is a nurse-educator who spends much of her life informing men and their spouses/partners about the possible consequences of treatment for prostate cancer; in particular she talks about the need for men to “come to terms with an altered way of being a man”
    An educational piece prepared by prostate cancer patients with support from professionals through the Michigan Cancer Consortium deals very specifically with the issue of “feeling like a man” after prostate cancer treatment.

    Arthur would just point out that there is one other thing that may be necessary here too, which is that someone in the family who he respects and would be prepared to listen to may need to sit down with your brother and tell him that he needs to do something about the problem. That may be hard, but it may be important.

  67. Dear Arthur,

    Thank you so much for your opinion. I’ve cancelled my appointment with Patrick Walsh, MD, at Johns Hopkins for prostate removal with nerve sparing. I’m sending my information to Dr. Walser, MD, in Texas. I think the laser ablation using 3 tesla MRI is a excellent choice. It exposes me to no radiation and can be monitored with two MRIs per year. It’s a start, and I think the best place for me. … Thank you so much for your help. I greatly appreciate it.

    Ron Rosen, MD

  68. Hi Arthur,

    Last August, I wrote to you with questions about the usefulness of the ultrasensitive PSA test and appreciated your opinion that in my case you saw no need to rush to radiation yet. Recently, however, there have been several posts on the InfoLink describing new research relevant to decisions about early salvage radiation therapy (e.g., Kang et al.). I’m wondering if this new information changes your view of my situation. By way of review, I am a relatively healthy 67-year-old who had a prostatectomy 20 months ago; my pre-surgery PSA was 9.278. My post-surgery pathology report was unfavorable: Gleason 3 + 4 with tertiary 5, pathological stage pT3a with focal extracapsular extension, negative surgical margins although some very close. Eight post-surgery PSA tests at 2-3 month intervals show a slow but steady rise from an initial 0.009; the last 3 levels are 0.032, 0.036, and 0.041; my PSA doubling time is 9.18 months. Currently, I feel fine, have relatively minor urinary and sexual side effects, and find myself resistant to potentially complicating my lot with toxic radiation. Originally, I thought I would have radiation when my PSA reached 0.2, but perhaps it is time to act now. I would appreciate your opinion.


    Arthur responded as follows:

    Dear Ray:

    Arthur says that, despite all of the recent and very reasonable discussion about exactly when we might be able to tell that a rising PSA post-surgery is indicative of heightened risk for a clinically meaningful biochemical recurrence, what we still do not know is whether having salvage radiation therapy when a man has a rising PSA that has reached (say) 0.05 ng/ml is any more beneficial than having such salvage therapy when his PSA rises to 0.10 ng/ml or 0.20 ng/ml. Worse still, is the fact that it may be several years yet before ongoing clinical trials can give us an accurate answer to this question.

    All that Arthur can really tell you is that this is a discussion that you need to have with your doctors very specifically in the context of your individual case. Could there be a benefit in having salvage radiation either now or when your PSA reaches 0.10 ng/ml as opposed to when it reaches 0.2 ng/ml. Arguable, yes … maybe. But no one can tell you that with certainty, and so in the end this is a matter that is entiorely in your hands to decide for yourself with the best medical advice available that is specific to you.

  69. My husband had a radical prostatectomy 15 years ago at age 62. His Gleason score was 9 (4 + 5) involving both right and left lobes. The tumor extended to the inked outermost aspect of the right prostate lobe. No extracapsular extension was identified. His PSA for years was “virtually negligible”; then 3 years ago it began rising to 0.08 to and then to 0.15 about 9 months ago. This week’s test indicates it is now 0.27. He is getting a PET scan in 8 weeks since there are two small nodules on his lung and will see his urologist again to review the results and will get another PSA test. What are his options? He is an active 75, in great shape.

    Thank you!


    Arthur responded as follows:

    Dear Barbara:

    Arthur says that he thinks that it is near to impossible to evaluate your husband’s options until there is some clarity over exactly why his PSA is rising. For example, the nodules on his lung may or may not have anything to do with prostate cancer. If they do, that is a serious problem. If they don’t, then one has to ask where the cancer is recurring and if that can be determined.

    With a PSA doubling time of the order of 9 months, it is likely that something is going to need to be done. If one can actually identify specific lesions, it may be possible to treat these directly in some way (but it also may not; it depends exactly where they are).

    Arthur would also note that if the nodules on your husband’s lung show no sign of being prostate cancer metastases, then the next question is whether the PET scan shows any other suspicious area. However, you do need to appreciate that your husband’s PSA level is still well below what people at places like the Mayo Clinic consider to be an acceptable level for an accurate choline-C11 PET/CT scan, so it may be very hard for anyone to make accurate determinations of risk based on your husband’s PET scan result.

    If there is any reason to believe that your husband’s recurrence is solely confined to the area where his prostate was originally situated (the so-called “prostate bed”), then radiation of that area is certainly still an option. On the other hand, if there is no clarity about where the cancer is recurring, then it might be better to consider a short course of androgen deprivation therapy (ADT, also known as “hormone” therapy) for 6 or 9 months. If this dropped your husband’s PSA back down into the undetectable range, then he could stop the ADT again and see how long his PSA stayed down in or near to that undetectable range.

    However, as Arthur indicated above, you will need to take one step at a time here and then evaluate the findings carefully with his doctors. The first question is going to be what the PET scan actually shows, and with what level of accuracy. Be very sure to ask the doctors just how accurate they think the results really are (i.e., how specific and how sensitive the test is in providing accurate data on which they can make reliable clinical recommendations).

  70. Hi Arthur,

    Just read the article “Biochemical recurrence among pT2 patients with a positive surgical margin post-surgery”. I see the 5-year biochemical recurrence-free survival is favorable for Gleason 6 and Gleason 7 (3 + 4) prostate cancer patients. I’m wondering … do all of these patients eventually experience a biochemical recurrence in their lifetime at some point because of the positive surgical margin leading to salvage treatment?


    Arthur responded as follows:

    Dear Mike:

    Arthur says, “No, absolutely not!

    Many patients with Gleason 3 + 3 = 6 and Gleason 3 + 4 = 7 disease and a small positive surgical margin after undergoing first-line surgery for localized prostate cancer will never experience a recurrence in their lifetimes — even if they live for another 30+ years. As far as we can tell, many such patients really are cured.

    The size or the numbers of positive surgical margins, and the Gleason grade of the tumor in that positive margin may well be factors that affect the risk for biochemical recurrence when there is a positive margin, however.

    Arthur would point out that it is precisely because forms of apparently localized prostate cancer exhibiting relatively low risk and favorable intermediate risk do so well after surgery that we have also now confirmed what many had thought for years — these same patients may, in fact, do do very well indeed without any form of treatment for many years if they are just monitored on active surveillance protocols.

    Arthur believes there is now an increasingly strong argument that the majority of men initially diagnosed with very low-risk, low-risk, and favorable intermediate-risk prostate cancer would be wise to just monitor their cancers until it becomes clear that they need treatment (as opposed to rushing into early treatment). Why? Because in a significant percentage of cases they will never actually need treatment at all, and in almost all the other cases they will do just as well with deferred (i.e., later) treatment as they would have done if they had had immediate treatment — but they may gain years of quality of life before having to deal with the side effects and complications of such treatment. It is true that there are men who simply can’t “cope” with the knowledge that they are living with an active — albeit low-risk — cancer. Those men may well prefer earlier treatment, but as Arthur moves inexorably towards his 70th year on the planet, he is increasingly of the opinion that he would defer his own treatment should he be diagnosed with low-risk or favorable intermediate-risk prostate cancer.

  71. I had brachytherapy a little over 3 years ago and after the first month have not ejaculated once. I get erect and go through the motion and feel that I am ejaculating but nothing comes out. It is a dry ejaculate. Why?


    Arthur responded as follows:

    Dear Jerry:

    Arthur says this is almost certainly because the brachytherapy was highly successful and killed off all of the cancer tissue in your prostate and all of the normal prostate tissue too. However, normal prostate tissue is necessary for the prostate to function normally … as the mechanism that pumps fluid and sperm out during the process of ejaculation. No living prostate tissue, no capacity to ejaculate, and so a dry orgasm.

  72. Hi Arthur.

    RP (with small positive margin, Gleason 3 + 4, grade 3 at margin’s apex) on August 16, 2012. Subsequent PSA results every 2 months following surgery: < 0.05, < 0.05 undetectable standard psa test, then 0.028, 0.030, 0.030, 0.040, 0.033, 0.038, 0.047, 0.055 detectable using the ultrasensitive PSA test at local hospital laboratory!

    I decided to call the hospital's lab just to see how often they calibrate their machines because my urologist was suggesting salvage radiation and, to my dissatisfaction, the supervisor couldn't answer that question. I understand when testing for PSA you should use the same laboratory and the same method of testing all the time but I wanted to be sure before I decided on salvage radiation. I switched to Quest Diagnostics using an ultrasensitive PSA (Beckman Coulter DXI method) and my last three results at 2 months apart were 0.04, 0.04, and 0.05. Your thoughts?


    Arthur responded as follows:

    Dear Orson:

    Arthur says that, in his humble opinion, if your PSA has managed to struggle from < 0.05 to 0.055 ng/ml (at its very highest) over the past 30 or so months, then you still have — to all intents and purposes — a PSA that is "undetectable" in any classical sense. If it was to suddenly jump to something like 0.1 ng/ml or higher, then there might be something to worry about, but Arthur can't in all honesty see anything for you to be worried about at the present. And Arthur also can't see any good reason to be getting salvage radiation therapy based on these data. Your PSA simply isn't rising fast enough (in Arthur's view) — but that's your decision in consultation with your doctors.

    Arthur would also ask why anyone seems to think it is necessary for you to be having PSA tests every 2 months. You really only need them every 3 months, and if your PSA is still < 0.1 ng/ml in another 30 months' time, you probably don't need them any more often than every 6 months.

    Arthur would point out that if your PSA was to go on increasing at its present rate (which appears to be a PSA doubling time of the order of about 16 to 18 months), then it might reach something like 10 to 15 ng/ml in 12 years from now, even if you do nothing at all.

  73. PSA jumped to 14; biopsy showed Gleason 5 + 4 = 9. After surgery. pathology report showed cancer out of the prostate gland; PSA up to 16. Radiation took PSA down to 2, which later jumped back up to 8. Have been on Lupron every month continuously; did Zytiga and took PSA back down to 2 but then went back up to 7; started Xtandi and after three doses ended up in the hospital due to severe side effects; started chemotherapy with docetaxel for 6 months and PSA dropped to 2 again, but is now going back up. In the meantime cancer has spread to the pelvic area, several small places in the abdomen, a larger tumor near the kidneys, and two tumors next to the heart.

    At this point, now what do we do?

    Don T


    Arthur responded as follows:

    Dear Don:

    Arthur says, “Good question!” Here is what little Arthur knows about what can be done in cases like yours:

    (a) Some men will respond to a second round of docetaxel chemotherapy.

    (b) Some men will respond to second-line chemotherapy with cabazitaxel (Jevtana), and this can have a small survival benefit.

    (c) Some men respond quite well to the injectable radiotherapeutic agent Xofigo (radium-223), and this can have a small survival benefit, but this may not be an option because of your soft tissue metastases.

    (d) At this time there is no known form of treatment that can induce a survival benefit after treatment with Zytiga, Xtandi, docetaxel, Jevtana, and Xofigo. But …

    (e) There are some investigational drugs like galaterone and olaparib that may (maybe) offer some benefit if you can find a clinical trial that is offering treatment with a drug like this.

    Arthur is all too well aware that this is not the most promising catalog of opportunities …

  74. Thanks Arthur. This is about what I expected. There gets to be a point where the quality of life is much less than the quality of death and continuing these darn medications is more debilitating than just letting nature take its course with the exception of pain control. I’m at ease with the world and myself and going over to the other side is not a bad thing but a release from the trials and tribulations of existence on Earth in this present form.


    PS: If you have any spare miracles available please send me one.


    Arthur responded as follows:

    Dear Don:

    Arthur promises to keep a close eye out for any miracles that he can spot!

  75. Hello Arthur,

    67 years old, with exposure to Agent Orange. The males in my family usually live into their 90s. I have no heart problems (carotid duplex 100% open) or diabetic issues and my BMI is below 24. I quit smoking (less than ¼ pack a day) 3 years ago.

    Diagnosed March 2015.

    Biopsy done after DRE and PSAs of 3.1 on 04/10/2012, 10.07 on 09/19/2014, and 10.81 on 01/28/2015.

    Biopsy report:

    A. Benign prostatic tissue (prostate, right apex, biopsy)
    B. Benign prostatic tissue (prostate, right mid, biopsy)
    C. Adenocarcinoma, Gleason score 3 + 3 = 6, involving 1 of 2 tissue cores and approximately less than 5% of total tissue (prostate, right base, biopsy)
    D. Adenocarcinoma, Gleason score 3 + 4 = 7, involving 2 of 2 tissue cores and approximately 60% of total tissue, 20% grade 4 (prostate, left apex, biopsy)
    E. Adenocarcinoma, Gleason score 3 + 4 = 7, involving 2 of 2 tissue cores and approximately 20% of total tissue, 10% grade 4 (prostate, left mid, biopsy)
    F. Benign prostatic tissue (prostate, left base, biopsy)
    G. Benign prostatic tissue (prostate, right anterior, biopsy)
    H. Adenocarcinoma, Gleason score 3 + 4 = 7, involving 2 of 2 tissue cores and approximately 70% of total tissue, 20% grade 4, with perineural invasion
 (prostate, left anterior, biopsy)

    I am still not clear as to what the “clinical stage” is given my results. Do you have any thoughts?

    I do not have nearly the problems of many on this Q&A, but am concerned nonetheless. And it seems that the more I research I do, the more confused I get. At present I have full bladder control and 100% erectile function. So, as everyone else wishes I’d like an effective treatment option and the best chance of retaining bladder and erectile function…mostly bladder control.

    I thought, given the options, it seemed as though brachytherapy would be the way to go, but am wondering about the difference between HDR vs low dose. Is there much difference in their side effects and do you think there are other treatment options I should consider?

    Thanks in advance, and thank you for coming out of retirement.

    Larry Anderson


    Arthur responded as follows:

    Dear Larry:

    Arthur says that at 67 years of age with a significant amount of Gleason pattern 4 disease in at least one biopsy core (core H), it seems highly likely that you are going to need treatment at some point in time. And there are going to be plenty of people that would suggest you need that treatment as soon as reasonably possible.

    With regard to your clinical stage, Arthur recommends that you call your urologist’s office and simply ask. Your clinical stage depends on exactly what was found on your DRE and/or what may have been visible on ultrasound when you had your biopsy. If your DRE was normal (i.e., negative), then you are clinical stage T1c. Click here for additional discussion of clinical staging.

    With respect to “the best” forms of treatment for someone like you … Arthur wants to emphasize that no one can make you a guarantee that any specific form of treatment will leave you with full continence and full erectile function that is as good as it was prior to treatment. And in all honesty no one can guarantee to you that a specific form of radiation therapy is more or less likely to have less side effects than any other. Why? Because so much depends on your personal anatomy and physiology, the skill and experience of the radiotherapy team, and simply whether “everything goes right” during the treatment planning and execution.

    So, given that information, Arthur would suggest that, at your age and given your clear focus on the post-treatment quality of your erectile/sexual and urinary functions, and the fact that you “only” have intermediate-risk prostate cancer:

    — Any form of surgery is probably a bad idea for you.
    — Any form of brachytherapy (including LDR and HDR) involves some degree of surgical intervention, and does come with real risks for short- and long-term side effects.
    — Some forms of radiation therapy really should be effective and may well come with lower risk for side effects (possibly including proton beam radiation therapy and stereotactic body radiation therapy — e.g., CyberKnife radiation, in addition to modern forms of IMRT), but all forms of radiation therapy are associated with loss of erectile/sexual function over time and can come with urinary tract complications too.

    At the end of the day, the most important thing is to find the most skilled radiotherapy center that you can — one where the physicians see a lot of prostate cancer patients and treat localized prostate cancer like yours day in and day out. Arthur cannot tell you that any one form of radiotherapy is more or less safe than any other. We don’t really have that data. What Arthur can tell you is that the skill and experience of the treating physician and his/her support team is paramount in minimizing risk for side effects while maximizing the probability of effective elimination of the cancer.

    Finding such a center and getting treatment there is likely to depend both on where you live and on the resources you have available to travel to known, high-quality centers.

  76. I read this very informative sight from time to time. My bona fides to comment are in 2011 and a few comments thereafter. I had a robotic radical prostatectomy back then (age 53 at the time). Larry’s query caught my eye. My two cents:

    (1) Listen to Arthur over all others. (He has no “skin in the game” and offers excellent, calm, level-headed advice).

    (2) I wish I had Larry’s situation, 67 years old and 100% control over bladder and erectile function (10 years before I am Larry’s age).

    (3) Have you considered doing nothing? I am not kidding. Arthur himself describes your situation as “intermediate risk” prostate cancer; I am sure you have heard the adage “more men will die with prostate cancer than from it”. … Prostate cancer often (usually from what I can tell) “grows” very, very, very slowly. Most men never know they “have” prostate cancer is my guess.

    (4) I would be very, very careful if I were in Larry’s shoes about doing anything. He sounds like a very bright guy who has taken care of himself. I feel sure of this: … there is a healthcare professional out there more than willing to “treat” Larry. The real question is — does he need it? I suggest most likely — NO.


    Arthur responded as follows:

    Dear Hobie:

    While Arthur does appreciate your confidence in his “excellent, calm, level-headed advice” (which he most certainly does try to offer, to the greatest extent possible), Arthur also feels that it is very important to make it clear that every patient is different — in many ways.

    Specifically, in relation to Larry:

    (1) Is it possible that Larry could “do nothing” (or perhaps more appropriately just carefully monitor his cancer using active surveillance)? Well, yes, perhaps, for a while. But as Larry points out, his life expectancy based on family history is somewhere into the early 90s, and we have absolutely no data at all suggesting that a man with prostate cancer, a PSA of 10 ng/ml, and three biopsy cores of Gleason 3 + 4 = 7 would be able to just monitor such a cancer for another 20+ years. In fact, that is extremely unlikely. If Larry’s life expectancy was another 5-6 years, it might be worth taking that risk. With a life expectancy of another 20 years, Larry is in a whole other place!

    (2) Many, but far from all, prostate cancers do grow very slowly indeed. However, the Gleason score is an indicator of aggressiveness, and a Gleason score of 7 is a “borderline” indicator of aggression which can strongly suggest the need to “do something”. Exactly what becomes a very personal decision.

    (3) It is Arthur’s entirely personal opinion that Larry has some time to come to a good decision about what he wants to do; that he might be able to just monitor a cancer like his for a year or so if his PSA was to be stable to 10 ng/ml; but that sooner rather than later he will probably need treatment of some type, and that he is absolutely correct in his estimation that (for him) the trick will be to find the very best treatment available (i.e., a treatment that maximizes the likelihood of eliminating the cancer and minimizes the risk for complications and side effects). Arthur’s only other key point in relation to this is that who carries out the treatment is a key part of that equation.

  77. To Arthur and Hobie,

    Thank you both for your input. I do feel that I need to take care of this given the rather rapid increase in PSA and the biopsy results (H core).

    A lot has happened in the 20 hours since my post and I’m nearly blind from the volume of reading I’ve done.

    The biopsy was performed by the VA in San Francisco and I have access to UCSF facility and surgeons. Post-biopsy the surgeon I spoke with said both surgery and radiation had equivalent success rates treating the cancer and that it was a process of choosing the side effect.

    Talked with my internist of 20 plus years. A brilliant diagnostician that I trust above all other medicos. I asked what he would do and he referred me to a urologist in his group that he knows and trusts.

    Talked with the other urologist and he gives it a T2a using DRE only.

    I’ve decided to investigate HIFU. Although I wince at the out of pocket expense, I could receive more conventional follow-up at no cost if the procedure is unsuccessful. I’m aware that there are still possible side effects, but the urinary incontinence rate is somewhat less. Given that I feel I have a long way to go in the aging department my post-procedure QoL is very important to me. There is a urologist in my area that has done over a hundred HIFU procedures and assisted with a hundred more.

    I’m well aware of the lack of clinical trial results, but willing to be a bit of a guinea pig given the anecdotal evidence. I would be interested in any thoughts you have on this subject.




    Arthur responded as follows:

    Dear Larry:

    Arthur notes that you joined the InfoLink social network and got some feedback about HIFU from the sitemaster there. All that Arthur can really tell you about HIFU is that he would also have referred you to the same data source as the sitemaster for the social network did (and the ensuing discussion on that page). There has been a lot of hype about HIFU, and there is no doubt that some patients do extremely well. However, the lack of any good data from any well-controlled clinical trials is something Arthur worries about a lot (just has he always has in relation to the early use of a whole bunch of other types of treatment over the years, none of which have ever actually measured up to the initial hype).

    If you think the specialist you have been referred to has sufficient experience and you want to take the risk, Arthur certainly isn’t going to tell you not to get HIFU. These are always very personal decisions. You just need to go into them with “eyes wide open”. After 20+ years Arthur has learned that very, very few new techniques for the treatment of prostate cancer are ever really as good as their early users like to believe.

  78. Thanks Arthur, I really do appreciate your input.

    I think I’ve read everything on this site (and others) re HIFU including the link Mike provided on the Social Network site. I guess my possible leap into this treatment is the result of the small set of friends and acquaintances that have had treatment (none HIFU). In that set urinary problems are about 50% (higher if including stress incontinence) and ED at 75% and rising. Given the results of the non-comparable treatment assessment in the PCRSG and the lack of any guarantees with any of the treatment options, I guess I really don’t see HIFU as more of a risk.

    As I feel I have a little time before making a decision, I will continue to read myself blind.

    Any further comments by you or anyone else are more than welcome. I need all the help and information I can get.

    Again thanks,

  79. Would this gentleman be a candidate for focused laser ablation?


    Arthur responded as follows:

    Dear Gmac:

    With six biopsy cores positive for cancer of Gleason 3 + 4 = 7, spread through both lobes of his prostate (not to mention the other positive cores with Gleason 6 disease), Arthur says there is no way that he would think this patient was a candidate for focal therapy of any type.

  80. My sincere best wishes Larry and, as I said, listen to Arthur above all others. My slight cynicism on this prostate subject stems primarily from two places:

    (1) From my reading it appears that very good healthcare professionals are still vigorously debating the merits of the PSA test. … Should it be performed and are the results of the PSA indicative of, well … anything? There is little doubt that many view the prostate as the most over-treated malady out there. Very good doctors are of the opinion the PSA test and the resulting treatment is often more harmful than beneficial. Or at least it sounds that way to my uneducated eye.

    (2) From December 2010 until my RP in March of 2011 I was treated at what was then known as the Malizia Clinic (in Atlanta). I am a lawyer so I know “how” to say what I am about to say. Anthony Malizia performed my biopsy in December 2010 — Gleason score 9; robotic RP 4 months later by one of his partners. I have no reason to doubt the biopsy results, except any doubt created by the following. (If interested, Google (and find out) what Anthony Malizia did to himself later that year … it is all over the net.) The Malizia Clinic is now called the Jenkins Clinic (or at least it was last time I looked in 2012). So forgive me if I seem a bit cynical on this prostate subject. The demise of Anthony Malizia was unfortunate — and for me untimely — as I now tend to question/doubt more than ever the “advice” on this subject. Ask Arthur is, in my opinion, the most credible source out there. I realize the above is my personal experience and may have little relevance to any others out there.

    I am doing well now (did have hernia surgery in October of 2011 — likely the result of the robotic RP) and perhaps I was treated properly … probably was is my best guess. Nevertheless, I have some nagging doubts about this entire prostate business. Best wishes to all dealing with this complex issue.


    Arthur responded as follows:

    Dear Hobie:

    The continuing discussion of the “merits” of the PSA test is in no way about the test itself. It is about when and in whom it is valuable to use it. Even Arthur is of the opinion that, over the past 30 years, its value has been vastly over-emphasized, and Arthur is extremely clear in his own mind that that is one of the reasons that large numbers of men received (and still do receive) aggressive forms of treatment for low-risk forms of prostate cancer that almost certainly did not need aggressive treatment immediately … and might never have received treatment at all. Over those past 30 years, there is absolutely no doubt that prostate cancer has been seriously over-treated. Almost every skilled urologic oncologist Arthur is aware of would now agree with that (and so would the majority of urologists and patient advocates).

    The evolution of active surveillance as a management strategy for low-risk disease is, in Arthur’s opinion, one of the most important developments in the management of prostate cancer since Walsh and colleagues developed the nerve-sparing radical prostatectomy (which is an excellent operation when carefully carried out in the patients who really need it, as opposed to the patients who could simply be monitored).

  81. Arthur,

    Is it possible for someone to have a PSA that’s higher than normal, say in the 6-7 range, that’s not due to cancer, BPH, or irritation? In others words, can some guys just have a high PSA?



    Arthur responded as follows:

    Dear Rick:

    Arthur says that here is always a medical/scientific reason for an elevated PSA level … but what that reason is can be very difficult to tease out in some patients. The commonest reasons for an elevated PSA are an enlarged prostate (BPH), an active urinary tract infection (including acute prostatitis), chronic prostatitis/chronic pelvic pain syndrome (CPPS), other forms of inflammation of the prostate, the presence of prostate “stones” (calcifications, like kidney stones), an actual injury to the prostate, and a whole range of other less common causes.

    Arthur is not aware that anyone “just has a high PSA level”. If that was the case, it would be relatively common to find PSA levels of 6-7 ng/ml in young, adult males in their 30s and 40s … but it isn’t. However, as we all age, the structures of our prostates can change. All that a PSA level can tell you and your doctor is the amount of PSA that is “leaking” out of your prostate and into your blood stream. There can be dozens of possible reasons for this.

  82. Question for Arthur: I had an RP followed by 33 sessions of radiation some 10 years ago. My latest PSA score was 2.9 which is the highest it`s ever been post-RP. I never reached a “cure” PSA score but my PSA has risen ever so slowly over the years, with two exceptions when it went down unexpectedly (when I was using Salvestrol). Your thoughts?

    Arthur responded as follows:

    Dear Don:

    Arthur says that given your apparent history over the past 10 years, the important thing is not any one absolute PSA level, but rather your PSA doubling time (e.g., how fast your PSA is going from 2.3 to 2.9 to 3.5 ng/ml).

    If you know your last three or four PSA test results and the exact dates that blood was drawn for those tests, you can enter them into the PSA doubling time calculator on the Memorial Sloan-Kettering Cancer Center web site. If your PSA doubling time is 18 months or longer, Arthur doesn’t think there is anything significant for you to be concerned about at this stage. On the other hand, if your recent PSA doubling times are more like being 12 months of less, then you may want to talk to your doctors about when they think some sort of intervention might be appropriate.

    Arthur doesn’t think that you can place too much significance on the effects of the salvestrols. Lots of different agents can make a man’s PSA level go down for a while — but that doesn’t necessarily mean that they are having a significant therapeutic effect of any type. We have no strong evidence at all that salvestrols are actually effective in the management of prostate cancer.

  83. Hi Arthur,

    I have written you from Türkiye about my father’s too high PSA level. He is 68 years old and prostate cancer history had started 11 years ago. We had used cabazitaxel, Zytiga, and some previous agents for his cancer. His PSA level has increased every PSA test nowadays (800 to 900 to 1200 to 1800 and now 2044). He has also soft tissue and bone metastases. We have never taken radiotherapy yet. I have three questions about my dad:

    (1) Is there any way for decreasing this PSA level?
    (2) Can radiotherapy reduce this PSA?
    (3) Do you know anything about atomic treatment with Lu-177? (Also it is called radionucleide therapy)?


    Cem …


    Arthur responded as follows:

    Dear Cem:

    Arthur says he is sorry to hear that that your father now has seriously progressive, castration-resistant prostate cancer. Exactly how much can be done to palliate and manage a prostate cancer like this is very difficult to know … but there really are not a lot of meaningful options.

    You could certainly ask his doctors about trying a drug like radium-223 diacetate (Xofigo), which is an injectable, systemic form of radiation therapy. It might be able to lower your father’s PSA levels for a while, but Arthur certainly couldn’t promise that. One also has to be a little careful about the use of this drug in men with serious soft-tissue metastases. However, Arthur knows of no other type of approved radiation therapy that would help, because it is clear that your father’s disease is too widespread.

    You ask about Lu-177, and Arthur assumes you are referring to an investigational form of treatment using lutetium-177-labeled anti-prostate-specific membrane antigen monoclonal antibody. There are some published data on the use of this agent (see, for example, this link), but Arthur thinks it may be very difficult indeed to get an agent like this in Turkey … especially outside a clinical trial. If you can get hold of it, then it might well be worth trying for your father — but I think even the effects of a drug like this would be limited in a man with your father’s level of disease progression, and you do have to be cautious about the myelosuppressive side effects.

    The single most important thing to be done with your father is to make sure he is in as little pain as possible, so I hope that his doctors are helping you to do this.

    Arthur wishes that he had some more helpful ideas to offer you, but unfortunately he doesn’t.

  84. Hi Arthur.

    Can HG-PIN itself raise total PSA levels and lower free PSA levels?


    Arthur responded as follows:

    Arthur is not aware of any evidence that HG-PIN on its own (i.e., without the presence of any benign prostatic hyperplasia or prostatis or other form of prostate problem, such as calcification of the prostate or prostate cancer) is capable of having any effect on PSA levels at all. Conversely, there are several things other than prostate cancer that can contribute to effects on PSA and %Free PSA levels.

  85. I am a 64-year-old with PSAs that are not significant, going from 1.7 to 2.7 over the past 10 years, with the last one being 2.5.

    I went to a free screening and they did the blood draw resulting in the PSA of 2.5. The urologist also did a rectal exam and said he could feel the perimeter of my prostate on the right side but could not feel it on the left. He suggested I get another urologist in his group (who does more prostate work) to have a look. After another DRE, that urologist said that he agreed with the previous urologist. He also said there was no urgency because of the relatively low PSAs but he suggested a biopsy.

    I called and spoke to his nurse and suggested an MRI to see what the prostate looked like. That is where we are. I know there is no guarantee that low PSAs mean no cancer. Am I following a good path and what else would you recommend.


    Arthur responded as follows:

    Dear Fern:

    Arthur says that at 64 years of age with a PSA that has been relatively stable in the range between 1.7 and 2.7 ng/ml for the past 10 years, he would be more concerned that you are at far greater risk for being diagnosed with a clinically insignificant and indolent form of prostate cancer than you are of not being diagnosed with a clinically significant prostate cancer. That would especially be the case if you have no other clinical reasons to think you might be at risk for prostate cancer or if there is no family history of prostate cancer among close male members of your family.

    Rather than having a biopsy at this point in time Arthur thinks that the MRI is a good idea and that you should get a repeat PSA and a %free PSA test (which can be helpful in differentiating between risk for prostate cancer and risk for other prostatic disorders) before seriously considering a biopsy. Arthur does not know whether either the Prostate Health Index test or the 4KScore test are available in the UK. If one or other of these tests is available, they are even better than a %free PSA test at differentiating between risk for prostate cancer and risk for other prostatic disorders, so it might be work asking the nurse at your urologist’s office if she knows if either of these tests are available.

    It is true that prostate cancer can occur in men with low PSA levels. However, Arthur would point out that this is relatively unusual. Arthur would also note that he is rather unclear what the urologist meant when he told you that he could “feel the perimeter of my prostate on the right side but could not feel it on the left.” That is an odd way to describe any type of DRE finding. Findings on DRE that are customarily associated with risk for prostate cancer relate to the clear presence of nodules or hard areas or rough areas on palpation of the prostate.

  86. Hello Arthur,

    This is Larry and I had the full ablation via HIFU last Friday the 5th. I was going to keep all apprised of the post-op progress good or bad. Is this where I should do it or should it be somewhere else?

    Thanks in advance,



    Arthur responded as follows:

    Dear Larry:

    If you want to keep other patients apprised of the effectiveness of your specific treatment, you would do much better to provide information like that through a site like either The “New” Prostate Cancer InfoLink’s social network (which has a group that is specifically designed for HIFU-related information) or through a site like Yananow.

  87. Thanks Arthur, will do.

  88. Arthur,

    I have two questions:

    (1) For someone on active surveillance, are there any PSA changes alone that should ever cause that person to come off of AS (to more aggressive treatment) or should the decision to come off of AS (to more aggressive treatment) only be driven by findings from biopsies and/or MRI’s?

    (2) If a 3 T prostate MRI read by experienced readers from a credible group (Massachusetts General in Boston) shows no evidence of any cancer, lesions, spots, marks — i.e. is completely clear, would that suggest that the odds of any significant cancer being present are very, very low?




    Arthur responded as follows:

    Dear Rick:

    Arthur says that with respect to question (1) in his recent review of “lessons learned” (which you might want to read) from his experience of managing men on active surveillance for about 20 years now, Dr. Laurie Klotz indicated that PSA kinetics are now used by the Sunnybrook group only as a guide to identify patients at a higher risk, but not to drive the decision to recommend treatment. This seems to be an increasingly accepted perspective, but there can always exceptions to every general rule.

    With respect to question (2), Arthur would certainly be of the opinion that a high-quality, multi-parametric MRI read by a skilled uro-radiologist that showed no signals of tissue at increased risk in a man who had previously been diagnosed with only a very small quantity of low-risk cancer in his prostate would be a pretty good indicator of minimal risk for significant cancer, but do be sure to discuss this with the relevant doctors!

  89. Thanks Arthur

  90. I had HIFU to treat my prostate exactly 5 years ago. I had Gleason scores of 6s and 7s and a PSA around 5.0. After surgery my PSA was 0.3 and over the past 5 years it has risen slowly. I had a fantastic result — full potency and no incontintence. This week my PSA was 0.8. My local urologist wants to do a biopsy. The surgeon who performed the HIFU said that it is not needed. The surgeon is pleased that my PSA is under 1.0 and said that he would not recommend a biopsy until my PSA was at 2.0 My local urologist is also certified to perform HIFU. Do you have any data of what my PSA should be 5 years after HIFU? Is this rise from 0.3 to 0.8 such a concern that you in my shoes would get a biopsy? I realize you are not a HIFU doctor, but you might have an opinion based on all your knowledge. Or someone out there who had HIFU 5 years ago may have an opinion. Thanks in advance!


    Dear Mr. Rizzo:

    It is Arthur’s understanding that there is no universally accepted set of criteria used to define biochemical failure after first-line HIFU. However, many leading specialists use the so-called Phoenix criteria (i.e., the patient’s nadir or lowest PSA level post-HIFU + 2 ng/ml; see for example this paper on outcomes up to 14 years post-HIFU). Based on that set of criteria, you are not in biochemical failure, since your PSA level is only 0.8 ng/ml, and you would only meet the Phoenix criteria for biochemical failure if your PSA rose to 2.3 ng/ml.

    Having said that, your real question here is: could you be exhibiting early signs of failure and if so what should you do about it?

    Arthur says there are two issues that may be highly relevant to answering that question. The first is your age/life expectancy. If you are still relatively young (60s or younger) and in good health, with a life expectancy of at least another 15+ years, the situation would clearly be very different from that in which you are in your 70s or older with declining health and a life expectancy of 10 years or less. The second is your PSA doubling time, which you can calculate by entering data from your last three PSA tests and their results into the calculator on the Memorial Sloan-Kettering Cancer Center web site. If your PSA doubling time is 24 months or higher, the situation is, again, very different from that in which your PSA doubling time is < 12 months.

    Arthur would suggest that if you are younger and healthier, then the potential benefits of an early biopsy are greater than if you are older and sicker. If you are younger and healthier and have a PSA doubling time of < 15 months, Arthur would also suggest that the value of a biopsy may be high. However, he would suggest two other things before you have a biopsy. The first would be to get a repeat PSA test done in a month or so's time (making sure to abstain from sexual activity for 48 hours before the blood draw), just to see whether the latest PSA result of 0.8 is an aberration. If the repeat PSA level is still 0.8 ng/ml or higher, then the second would be to talk to your doctors about having a multiparametric MRI so that any repeat biopsy could be done under MRI/TRUS fusion guidance, in which one is given a standard 12-core systematic biopsy along with a biopsy of any areas of the prostate that look clinically suspicious on the MRI.

    The potential benefit of such a biopsy is that you would have greater clarity about what you were dealing with and could make decisions about any next set of steps based on that data … as opposed to waiting in the dark for your PSA level to reach 2.3 ng/ml, which might happen in a year or might not happen for many years, if ever.

  91. Is there any research showing that dark chocolate helps in the treatment of prostate cancer?


    Arthur responded as follows:

    Dear Blanch:

    Arthur says that if there is any such meaningful research, he is not aware of it … but see here.

  92. Dear Arthur,

    I wonder if you are able to throw any light on the following reported in Science Daily just recently:

    German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)
    An agent called PSMA-617 is capable of attaching specifically to prostate cancer cells. This agent can be labeled with various radioactive substances. When chemically bound to a weakly radioactive diagnostic radionuclide, it can detect prostate tumors and their metastases in PET scans. If labeled with a strongly radioactive therapeutic radionuclide, PSMA-617 can specifically destroy cancer cells. A first clinical application of this radiopharmaceutica has now delivered promising results.

    This looks as if it might be really promising?

    Kind regards



    Arthur responded as follows:

    Dear Graham:

    Arthur says that PSMA-617 is one of several PSMA-linked products in development that may prove to have efficacy in the treatment of advanced forms of prostate cancer. However, exactly what level of efficacy is always difficult to determine on the basis of early stage trials. PSMAs have been tested in combination with a variety of different radioactive agents — in the case of PSMA-617 the radioactive agent is lutetium-177 (Lu-177). Here is a link to an article about the clinical results of a small Phase II trial using either the same or another very similar agent.

    Arthur notes that PSMA-linked products like this have been in development for many years (dating back into the mid 1990s). We are now seeing data from early stage clinical trials of these agents. However, as yet Arthur is not aware of a single randomized Phase III clinical trial (in prostate cancer or any other form of cancer) that might lead to product approval. See also this commentary about PSMA Lu-177 specifically and several of the other studies discussed here.

    While PSMA-617 and some similar products certainly show signs of activity in advanced prostate cancer, Arthur believes that we are going to need to see a good deal more data before it will be clear whether such products really do have high levels of effectiveness and an appropriate safety profile.

  93. Had cancer diagnosed in 11/07 and treated with radiation successfully. Have followed up with urologist faithfully. Saw urologist 7/17/15. His office called and reported PSA virtually undetectable and all fine.Is this normal? Not to have any PSA able to be detected?

    Thanks – Tom


    Arthur responded as follows:

    Dear Tom:

    Arthur wants to be quite sure he is understanding your question. He thinks you are saying that you had radiation therapy for prostate cancer in November 2007 and that following your most recent PSA test you were told over the phone that your PSA was undetectable.

    An undetectable PSA level after radiation therapy for prostate cancer is not common (although it can happen) unless you have also been having androgen deprivation therapy (ADT, also known as “hormone” therapy). Also, if you have been having serial PSA test results over the past 8 years that have been detectable (i.e., anywhere between about 0.1 and perhaps 0.5 ng/ml), it would be odd if you suddenly got a result that was completely undetectable.

    It is certainly possible that you were one of a number of people that the office was calling that day and that you were given someone else’s PSA result by accident. You may want to call the office back to check. Arthur obvioulsy doesn’t know what your last three or four PSA results had been before the most recent one. That information would help to clarify the possible situation.

  94. Just read about DNA-PKcs as possible basis for treating metastasis of prostate cancer. It sounds promising. Do you have any insights to share? Sure could use some hope here!



    Arthur responded as follows:

    Dear Uncle Fuzzy:

    Much as Arthur would like to be able to tell you, in no uncertain terms, that “DNA-PKcs inhibitors are the bees knees!”, unfortunately Arthur simply doesn’t have any evidence or insight yet to be able to make such a claim.

    As is almost invariably the case in the drug development process, until we have some data showing results from at least a Phase II trial it is almost impossible to make any good guesses about whether any product will actually work effectively and safely in the treatment of any form of cancer — let alone late stage prostate cancer.

    What Arthur does think you might be interested in doing, however, is seeing whether you could participate in a clinical trial of DNA-PKcs inhibition once we have information about one of these Phase II trials. That at least would give you an early shot at discovering whether such a product might work for you! Your ability to participate in such a trial will, rather obviously depend on the combination of where you live and where the study center(s) for the trial are located.

    Arthur is sorry that he can’t offer you any more positive insight at this point in time.

  95. Hi Arthur.

    Does a detectable PSA after surgery (0.05 , 0.1 or 0.2, whichever definition is used) ALWAYS progress to distant metastasis?


    Arthur responded as follows:

    Dear Mike:

    Arthur says the simple answer is “No”. There are (a) men who have low, stable PSA levels after surgery of (say) 0.15 ng/ml post-surgery who may never progress at all, and (b) men who have low PSA levels post-surgery that progress so slowly that they never have metastatic disease. In each of these cases, it is most likely that these will be men who had low-risk prostate cancer at the time of surgery (i.e., clinical stage T1c, a Gleason score of 6 or less, and a PSA level of 10 or less); however, this phenomenon can also be observed in men who had higher-risk disease.

    Arthur would advise you that the issue is not what the baseline PSA is immediately after surgery if it is < 0.2 ng/ml. The issue is whether the PSA is stable at that level or is rising so slowly that the PSA doubling time is (usually) more than at least 2 years, e.g., a PSA level that goes from 0.10 on January 1, 2015, to 0.15 on January 1, 2017, to 0.3 on January 1, 2019, etc.

    However, Arthur would also note that PSA doubling times may be long early and then speed up over time. It is therefore almost possible to make any absolute decision about risk moving forward that may not need adjustment over time.

  96. Truly informative and helpful.


    Arthur responded as follows:

    Dear Maggie:

    Arthur always appreciates knowing that he is being of a little help to people … so he thanks you for your kind comment.

  97. My doctor scared me into a prostate removal in 2008; radiation 2009; bladder stents 2009 to try and stop doctor’s mis-snip. PSA started rising in 2012 and got up to 11 in January 2015. They gave me shot of Lupron in April. My PSA subsided to less than 1 ng/ml in July. Now my testosterone level is above 167. Any idea what this means?


    Ron Potts


    Dear Ron:

    Arthur would need to know a lot more about the precise details of your initial diagnosis and about your treatment over time to be able to give you a really meaningful answer to this question.

    Having said that, Arthur thinks that: (a) you appear to be back in remission; (b) your serum testosterone level will probably continue to rise so long as you don’t need another injection of an LHRH agonist; (c) the first critical question is going to be how long you will be able to remain in remission before you PSA starts to rise slowly again; (d) the second critical question is going to be how fast your PSA rises if and when it does start to rise again and at what PSA level you and your doctors will decide it is necessary to have at least one more shot of an LHRH agonist.

  98. Is it possible to have bone mets with a zero PSA for 8 years?


    Arthur responded as follows:

    Dear Gary:

    Arthur says, “Yes.” It is certainly possible (always assuming that you are being treated with some form of androgen deprivation therapy). However, Arthur also thinks it would be somewhat unusual.

  99. What is bone mets?


    Arthur responded as follows:

    Dear Phil:

    Arthur says that the term “bone mets” is an abbreviation for “bone metastases”, which is a consequence of the spread (“metastasis”) of the original cancer out of the organ where it originally started (the prostate in the case of prostate cancer) to bones like the spine, the pelvis, the ribs, the shoulders, and later on the “long bones” of the arms and legs. In the case of prostate cancer (and some other cancers like breast cancer), bone tissue is a favored tissue for the spread of cancer, but it can also metastasize to other organs as well, such as the the liver, the lungs, and even the brain.

  100. Good morning Arthur,

    I have a question regarding statins.

    I have recurring prostate cancer with lymph node metastasis as identified by MRI with Fereheme and gadolinium as contrast mediums in 2010. Conventional CT and MRI do not indicate any nodal metastases.

    Since the completion of 81 Gy of IMRT in conjunction with ADT3 (Lupron, Casodex, and Avodart) in 2004, my PSA has risen from 0.003 to just under 4.0. I remain on Avodart (0.5 mg b.i.d.). Please note that a PSA of 4 while on Avodart is effectively a PSA of 8 as Avodart reduces PSA levels by approximately 50%.

    In the last 4 years, this increase fits an exponential curve, but in the last 6 months has leveled off in the 3.8-4.0 range. In order to control cancer growth, in addition to Avodart, I have added metformin ER 500 mg b.i.d., numerous supplements, and dietary modification (no red meat, no dairy, and no egg yokes). My blood glucose is under 100 so I am taking metformin due to the many reports indicating a benefit for prostate cancer rather than for control of diabetes.

    Recently my cholesterol has risen to 270. I know there have been several papers exploring the idea of statins being helpful in controlling prostate cancer in addition to the benefit of cholesterol reduction.

    Statins break down into: (1) water-soluble statins (rosuvastatin and pravastatin) and (2) lipophilic (lipid-soluble) statins (atorvastatin, cerivastatin, fluvastatin, lovastatin and simvastatin).

    It seems that the water-soluble statins are minimally metabolized by the cytochrome P450 enzyme system before elimination. Thus they do not participate in any clinically relevant drug interactions with CYP450 agents. Supposedly pravastatin improves insulin sensitivity. Rosuvastatin does not change insulin sensitivity; however, supposedly it can increase the rate of new onset of type II diabetes in a dose-dependent manner.

    The lipid-soluble statins may have interactions with other drugs that are processed by the CYP450 system and may also have adverse metabolic consequences that include impaired insulin secretion and promotion of insulin resistance.

    Is there one statin out there that you believe might have this benefit of cholesterol control without any (or minimal) negative side effects?


    Arthur responded as follows:

    Dear Tom50:

    Arthur wishes to be very clear that he is not either a pharmacologist or a medicinal chemist. You are asking a question that (Arthur suspects) even a highly specialized pharmacologist or medicinal chemist with years of experience in the development of statins probably can’t answer because it contains factors that are based on hypotheses as well as actual factual information. It also takes no account of how your personal metabolism may work (as opposed to the metabolism of the “average” 50-year-old male).

    Arthur also would observe that the effect of dutasteride (Avodart) on PSA levels, i.e., that PSA levels in men on dutasteride are roughly half those of PSA levels in men who are not on dutasteride, is only known to be true in men who have received no actual treatment for prostate cancer. The idea that it would be true in your case, after prior radiation therapy and ADT is entirely hypothetical.

    Third, Arthur would note that the diverse array of treatments that you have been using already makes it near to impossible to know whether adding a statin to your polypharmacy would have either positive or negative effects from a prostate cancer perspective. You already appear to be “managing your PSA” very effectively. Exactly to what degree such management of your PSA level represents meaningful management of your risk for progressive prostate cancer is a much harder question to answer.

    Having said all of that, a total cholesterol level of 270 places you at a significant and potentially serious risk for cardiovascular consequences. You do need to get your cholesterol level down. The normal way to approach this is to start by using a relatively low dose of a proven statin like simvastatin, atorvastatin or rosuvastatin. (Most of the others that you mention are not widely used clinically today because they are not as clinically effective at lowering total cholesterol levels.) Arthur suggests that worrying about the hypothetical added benefits of statin therapy on your prostate cancer is probably not as wise as focusing on getting your cholesterol level down into a healthier range, i.e., < 100, … and in the near future.

  101. Hi Arthur,

    I have written you from Türkiye about my father’s too high PSA level. He is 68 years old and prostate cancer history had started 11 years ago. We had used cabazitaxel, Zytiga, and some previous agents for his cancer. His PSA level has increased every PSA test nowadays (800 to 900 to 1200 to 1800 and now 2044). He has also soft tissue and bone metastases. (I had written about this on May 13, 2015.).

    After this question we started to use Lu-177 treatment; my dad’s pains were stopped by this treatment. We are going for a third treatment on September 10. After the first usage his PSA come down from 2,250 to 2,200, but after the second treament his PSA went up again to 2500. If this radionuclide therapy can’t stop the increasing of his PSA, how can we stop this. I’m waiting for your answer hopefully. …


    Arthur responded as follows:

    Dear Cem:

    As Arthur said previously, in answer to your message on May 13, he knows of no currently available treatments that can be used with any degree of serious likelihood that they can arrest the progression of your father’s disease. The only other drug that he is aware of that might be useful is radium-223 diacetate (Xofigo), using this drug in patients with serious soft-tissue metastases can be problematic, so only your father’s doctors would be able to advise you whether this is a possibility.

    Much as Arthur would like to be able to tell you that there are other forms of treatment available that would be likely to work to arrest your father’s cancer, there are no such drugs that Arthur is currently aware of.

  102. Sir:

    My father is 58 years old with a heart problem. His heart is 35% working. He has been suffering prostate problems for the past 3 years back. Now his prostate is 85%. Can you tell me what he should do?


    Arthur responded as follows:

    Dear Shally:

    Arthur is not a doctor and so no, Arthur can not tell you what you and your father need to do about his situation. And in any case, Arthur would need to know a lot more detail about your father’s situation to be able to comment sensibly.

    What Arthur can tell you, however, is that you and your father need to have a very serious conversation with someone who has no interest in treating his prostate condition (e.g., his cardiologist if he has one) about what his life expectancy might be based on his heart disease. With only 35% of normal cardiovascular function, your father’s prostate cancer may or may not be serious by comparison, depending on the exact details of the prostate cancer. However, your father is highly unlikely to be a good candidate for surgery for the prostate cancer; he is not likely to be a good candidate for long-term treatment with androgen deprivation therapy (ADT, also known as “hormone” therapy); and so the only common treatment for prostate cancer that is a real option may be some form of radiation therapy.

    Another factor that is important here is whether your father’s prostate problems are seriously affecting his quality of life — in terms of things like his ability to urinate and empty his bladder. Even if he has a limited life expectancy because of his heart condition, it will be important for him to have as good a quality of life as possible. If his prostate condition is affecting that, it may be possible for him to at least have treatment that will relieve any urinary tract problems.

  103. Hi Arthur.

    In 2012 I had a perineal biopsy which mapped the prostate. The cancer was contained in the prostate. I also had an MRI which confirmed the cancer was contained in the prostate. My Gleason score was 3 + 4 = 7. My PSA was 9.

    When the prostate was removed in January 2013 there was a large, cancer-free margin of tissue that surrounded the prostate. My PSA was 0.03 in 2014. In 2015 I had two PSA tests which were both 0.01. My last PSA was 0.06. I will have another test in 3 months. My doctor says the cancer is now active.

    My question is, seeing that every test came back saying the cancer was contained in the prostate, how is it now outside.

    Thank you,



    Arthur responded as follows:

    Dear John:

    Arthur thinks that there are two quite different possibilities going on in cases like yours, and he would urge caution before taking action as a consequence, but you do need to discuss both possible options with your doctors.

    The first possibility was that your cancer was not, in fact, confined to your prostate at all at the time of your surgery — potentially because a very small number of prostate cancer cells had already moved outside the prostate before you had your surgery and were not visible on MRI. This is not an uncommon situation. Arthur would note that when this happens the most common situation is that such a cancer has micrometastasized to the so-called “prostate bed” (the anatomical site where your prostate used to be located), and it can be very effectively treated most of the time by radiation therapy. However, …

    The second possibility, which is also relatively common, is that non-cancerous prostate tissue left behind by your surgeon has started to grow, thus producing enough PSA to be measurable. If this is the case, then you don’t have recurrent prostate cancer.

    Arthur would point our that, while your PSA is indeed rising, a formal definition of biochemical recurrence occurs in a patient treated surgically only when his PSA rises to 0.20 ng/ml. We do not have good data on the clinical significance of PSA doubling times in men with PSA levels of < 0.10 ng/ml. And furthermore, we have no data to suggest that localized radiation therapy for men with recurrent prostate cancer and a PSA level of < 0.20 ng/ml is any more effective than when their PSA actually reaches 0.20 ng/ml. (Having said that, if your PSA had gone from 0.03 to 0.01 to 0.05 to 0.09 over the same 2-year period, then Aurthur would think it was much more likely that you were, indeed, exhibiting biochemical recurrence.)

    In the end, what you want to do in a situation like this is a matter for discussion between you and your doctors, but, as Arthur noted at the start of this response, you may be wise to act with caution at first before deciding on any further course of treatment. The variations in your last four PSA levels are (arguably) well within the variations that could occur because of the nature of the test, and your next PSA level might well come back at 0.03 ng/ml again, in which case it would seem unlikely that you actually have biochemically recurrent disease.

  104. Many men who have been testing for some time with Quest Diagnostics and getting a < 0.1 PSA result now seem to be getting 0.1 instead. Is this the new "low-as-it-can-go" for Quest Diagnostics? I have called and e-mailed them with this question but have so far gotten no answer from them. Can you find out if this is Quest Diagnostics' new "low" for this PSA test?


    Steve F.


    Arthur responded as follows:

    Dear Steve:

    Arthur is sorry but he is in no better position than you are to get an answer to this question (Actually, he is probably in a worse position since he doesn’t use Quest for any personal laboratory testing.)

    Arthur would suggest that you ask your urologist to ask Quest this question. S/he is probably in a better position to get an answer from Quest’s medical staff.

  105. My husband’s PSA has consistently been 3.8 to 4.0 over the last 12 months. What’s the next step to take?


    Arthur responded as follows:

    Dear Vicki:

    While your question may seem like a simple one, actually it isn’t. The answer depends on a whole range of factors … starting with your husband’s age, whether he has any possible clinical indicators of risk for prostate cancer, what his PSA was before, and whether he has an of the other significant risk factors for prostate cancer.

    Arthur strongly suggests that you start by having a look at (a) this commentary on this web site and (b) the article by Wibowo et al. that is referred to in that commentary. If there is any good reason to think that your husband might be at clinically significant risk for prostate cancer, he would be wise to get a referral to a good urologist or (better still) a urologic oncologist and then ask that doctor about having either a 4KScore test or a Prostate Health Index/phi test prior to making any decisions about whether a biopsy might be necessary.

  106. Dear Arthur,

    Right now, I am facing a decision to do SRT only or SRT + ADT. I am anxious to get some advice from you.

    Brief history: Pre-surgery PSA was 42.4. Open radical prostatectomy was done February 2015. pT3aN0M0; margin positive; Gleason 4 + 4 (second opinion 4 + 3). Post-surgical PSA levels — 0.02 at 3 months; 0.05 at 6 months; 0.08 at 8 months. Radiation oncologist suggests that I should to do SRT but did not mention about ADT. I searched the Web and it seems to do both will get a better chances to be cured or have a better outcome. What do you think?

    Thanks a lot.



    Arthur responded as follows:

    Dear Andy:

    Arthur is not a doctor and so he cannot tell you what you need to do. What he can tell you is that you appear to have had four indicators for high-risk prostate cancer: your original PSA level being > 20 ng/ml; the positive surgical margin or margins post-surgery; extracapsular extension of the cancer (indicated by your clinical stage of pT3a); and a Gleason score of 4 + 3 = 7 or 4 + 4 = 8.

    In theory you are a good candidate for either simple salvage radiation therapy, or, as you have noted, salvage radiation therapy + a course of adjuvant radiation therapy (ADT).

    Arthur thinks that, if this was him who had this cancer, he would want to have a serious talk with his doctors about having a short course (4 or 6 months) of ADT starting 3 months prior to initiation of the radiation therapy. It may not be 100% necessary, but such treatment would increase the likelihood of putting a cancer like this into long-term remission (or maybe even eliminating it entirely).

    However, in the end this is your personal decision in discussion with your doctors. You should talk about both options to the radiation oncologist and to the urologist who has been managing your cancer since it was diagnosed (who may or may not be the surgeon who operatyed on you).

  107. Hi Arthur.

    On reading your forum and forums on the internet it seems that that a lot of men who have had a RP that within 2 to 5 years the cancer returns, so would it be better for a lot more men to have radiation and hormone treatment? I did read a article that said that for 50% of men who have had an RP that cancer returned or was still there when the prostate was removed.


    Arthur responded as follows:

    Dear John:

    As far as Arthur is aware, there is absolutely no good reason to believe that the long-term outcomes of men treated with radiation therapy plus androgen deprivation therapy (ADT) would necessarily be any better that the long-term outcomes of men treated with radical prostatectomy, assuming that we are talking about strictly comparable types of patient.

    The combination of radiation therapy + ADT is considered to be appropriate as first-line therapy only for carefully selected men with unfavorable intermediate-risk or high-risk, localized prostate cancer and men with locally advanced prostate cancer. Surgery alone, on the other hand, can be used to treat the same two groups of patients with full appreciation up front that additional, adjuvant or salvage radiation therapy is highly likely in a high percentage of such patients, together with at least a short course of radiation therapy in some of those patients.

    It is also important to remember, in Arthur’s humble opinion, that first-line use of radiation therapy along with ADT has two major drawbacks: (1) it eliminates, for most patients, any future chance of surgical treatment, and (2) it adds to the risk of initiating the early onset of androgen resistance.

    There are now several different types of first-line management for prostate cancer available, of which Arthur considers simple monitoring on active surveillance or watchful waiting to be among the most important and potentially valuable. Any interventional first-line treatment for localized or locally advanced prostate cancer needs to be carefully selected after careful evalaution of the individual patient and discussion of all his options with his doctors. There is no evidence, at present, that any one form of first-line therapy is definitively “better” that any other.

  108. Hi Arthur!

    Can HIFU be used instead of EBRT to treat prostate cancer patients with positive margins such as myself or is this just used as first-line treatment?


    Arthur responded as follows:

    Dear Mike:

    In Arthur’s opinion the appropriate range of uses of HIFU in the management of prostate cancer is still not very well defined at all. In theory, at least, it seems likely that HIFU could be used as a form of adjuvant treatment for men found to have positive surgical margins after a radical prostatectomy. However, how effective and safe HIFU might be in this use, Arthur is certainly not qualified to judge, and he knows of no published data regarding the use of HIFU in this manner.

    Arthur suspects that the only people qualified to answer a question like this would be one or two of the very small number of physicians with very extensive experience of the use of HIFU to treat prostate cancer … and even then Arthur has no idea how many of those physicians (if any) have any experience of using HIFU to treat positive surgical margins.

    In addition. Arthur would point out that there is no evidence as yet that any health insurance provider would cover this cost (although they might).

  109. Hi Arthur,

    My father, 56 years old, was diagnosed last week with Stage IV / D2 metastatic prostate cancer, which has spread to the lymph nodes in the abdomen. A 68Ga PSMA ligand PET/CT scan also reveals a single suspicious bone lesion. He has been advised to start immediate hormone therapy and prescribed degalerix (Firmagon). He has also been prescribed calcium supplements. I have three questions:

    (1) Should he be prescribed Casodex or an anti-androgen as well along with the degalerix? Wouldn’t that be helpful to ensure cancer cells don’t get testosterone?

    (2) Shouldn’t he be prescribed a biophosphonate like zoledronic acid to proactively address bone brittleness issues that come with ADT?

    (3) How would we come to know if his cancer is hormone-sensitive?

    Thank you so much!



    Arthur responded as follows:

    Dear Sankalp:

    Arthur says he is sorry to hear about your father’s diagnosis. Clearly he is going to need aggressive treatment to manage his condition.

    Arthur can give you specific answers to some of your questions and not such specific answers to others. So …

    (1) No, your father does not necessarily need to be treated with Casodex or another antiandrogen because degarelix is an LHRH antagonist (as opposed to being an LHRH agonist, like say Lupron or Zoladex). If his PSA level isn’t dropped down to < 0.1 ng/ml by the degarelix, it is possible that adding a drug like Casodex might be helpful then. However, your father could also ask his doctors to monitor his serum testosterone levels each time he gets a new PSA test. Ideally, his serum testosterone level should drop down to < 20 ng/ml, and it certainly needs to drop to less than 50 ng/ml.

    (2) Exactly when to start a newly diagnosed patient like your father with only a very small site of metastasis on a drug like zoledronic acid (Zometa) is not really very well defined. Arthur suggests that your father should raise that question with his doctors. It may or may not be a good idea if — with the exception of the single site of metastasis — his bones are currently strong, but he may well need to be started on a drug like zoledronic acid in the near future.

    (3) Arthur says you will know if your father is hormone-sensitive if his PSA level drops into the undetectable range (< 0.1 ng/ml) over the next month or so (actually this usually happens quite quickly with degarelix — within a week or two — if it is going to happen).

  110. Hi Arthur! Would hypofractionation be sufficient in treating men with positive surgical margins such as myself once recurrence is evident? I’m a little over 3 years post-surgery; PSA has been at 0.05 for the last 1.5 years.


    Arthur responded as follows:

    Dear Mike:

    Arthur says that the potential for salvage radiation to be administered using hypofractionated forms of radiation therapy is rather lower than for its use in the treatment of localized prostate cancer because it depends on precisely which tissues are going to need to get radiated.

    Arthur believes that in theory it should be possible to use hypofractionated forms of radiation as salvage therapy if such radiation really only needed to be administered to the prostate bed. However, if salvage radiation needed to be administered to a wider area of the pelvis, then this is less likely.

    As yet Arthur is not aware of any meaningful data on the use of hypofractionated radiation therapy in the salvage setting, and so he thinks this would really need to be a question you took up with the radiation oncologist should salvage radiation become a necessity for you. At present you appear to be doing well, based on your post-surgical PSA data, and so it is perfectly possible that there will be no need for salvage radiation anyway.

  111. Dear Arthur,

    I was 68 years when I was diagnosed for aggressive prostate cancer in February 2015 after a 12-core transrectal biopsy. I underwent retropubic radical prostatectomy in March 2015. Before surgery I did not have symptoms of any urological disorders except my PSA at that time was 11.7 ng/ml. My pathology report post surgery was as follows:

    1. Tumour type: Prostate adenocarcinoma (small acinar type)
    2. Histologic grade: Gleason grade 4, 5, and 3 present. Gleason sum score, 4 + 5 = 9
    3. Extraprostatic extension: Absent
    4. Lymph node invasion: Absent
    5. Seminal vesicles: Not involved; Vascular invasion: Absent
    6. Perineurial invasion: Present
    7. Surgical resection margins: The surgical resection margin is focally involved in the left lower pole. (The tumour is still within the prostate.) Apical resection margin is also involved focally.
    8. Tumour burden: Approximately 40% of the volume of the prostate is involved. Both lobes are affected.
    9. Maximum size of dominant tumour nodule: 12 x 10 mm.
    10. Pathological staging: T2N0Mx

    Post surgery up to now I am fully continent and also fully impotent. Considering my age I consider the latter as unimportant since a cancer-free life (if possible to achieve under the circumstances) is more important than anything else.

    My PSA level came down to 0.079 ng/ml 6 weeks after surgery and before any adjuvant treatment. From the 7th week (end April 2015) my urologist/oncologist advised me to start on Zoladex 10.8 mg and Calutide 50 mg (once daily). ADT to continue for 18 months (Zoladex injection every 3 months) and on October 28, 2015, I took the third shot.

    Whilst being on the ADT I started on my radiation therapy (IMRT-TOMO) from June 15, 2015. That is 3 months after the surgery and 1.5 months after starting ADT. Radiation comprised 38 sessions with a total dose of 74 Gy to the prostate bed. Radiation therapy was completed on August 5, 2015.

    PSA levels after ADT and IMRT:

    — 0.002 on June 6, 2015 (12 weeks after surgery and 5 weeks after ADT )
    — 0.001 on August 15, 2015 (5 months after surgery; IMRT completed; ADT + Calutide continues )
    — 0.003 on October 20, 2015 (on ADT + Calutide)

    Thus far no appreciable side effects to complain of. Meet the urologist/oncologist every 3 months for the Zoladex injection and a cool chat. (He is not bothered, I think since my PSA is undetectable.)

    I would appreciate if you could kindly answer my following questions.

    1. I can understand why I have been given ADT continuously for 18 months, Calutide and also radiation therapy from the very beginning post-RP despite very low levels of PSA could be because of my high Gleason score and the positive surgical margins. Yet I am asking you whether I am being over-treated with undue urgency without watching on the PSA behaviour.

    2. Do you think the radiation treatment I have received combined with the ADT would have eliminated the potential recurrence risk posed by the type of positive surgical margin mentioned in my pathology report?

    3. Taking into account the pathological status of my cancer and the treatment protocol I have followed proactively, do you think I can expect a cure or a long-term remission (say roughly how many years) in my prognosis?

    Thank you in advance.



    Arthur responded as follows:

    Dear Sisira:

    The only one of your questions that Arthur (or anyone else) can answer is the first one — about whether you have been over-treated. The answer to that is a definitive “No.” While you could certainly have chosen not to have the “immediate” adjuvant radiation therapy + ADT, Arthur’s opinion is that if you hadn’t had it you would almost certainly have required the same type of salvage treatment within a couple of years time anyway, and there is a strong argument that by having it immediately you have a greater chance of either a cure or at least a long-term remission.

    Arthur says that, with respect to your other questions, an answer is only going to be possible when you complete the ADT in about another 12 months time. If your PSA level then stays stable and down at its current level of < 0.01 ng/ml for about 12 months after you stop the ADT (i.e., about 2 years from now), then there is a good chance of either a cure or at least a long-term remission, but it is impossible to predict this with any accuracy at the present time using any nomogram that Arthur is familiar with.

    Arthur does not believe that the very small changes in your PSA level (between 0.001 and 0.003 ng/ml) since June are clinically meaningful. However, if your PSA was to start rising significantly while you are actually on ADT (to something like 0.10 ng/ml or higher) then there may well be a problem.

    There are certainly other men with Gleason 9 cancers and positive surgical margins who appear to have been either cured or placed in long-term remission using the treatment strategy that your doctor has recommended and implemented for you. Whether that will prove to be true for you as an individual, however, just cannot be predicted at this stage.

  112. Dear Arthur,

    Thank you very much for your prompt reply to all my questions. I shall be grateful to you if you can add more to your last paragraph regarding the risk posed by the “positive surgical margin”. As I have learned since of late the type of “positive margin” may vary from case to case. In my case it is described under item 7 of my above pathology report. When the tumour is confined to the organ which is focally involved is less significant compared with multifocal positive margins or extensively positive margins. What I am exactly asking is whether the 74 Gy radiation I have received on my prostate bed could have killed the malignant cells attached to the type of margin mentioned in my case. Being on ADT may also be taken into consideration.

    Thanks and regards



    Arthur responded as follows:

    Dear Sisira:

    Arthur says that you appear — based on your prior message — to have actually had two positive surgical margins (“The surgical resection margin is focally involved in the left lower pole. … Apical resection margin is also involved focally.”)

    The clinical significance of those positive margins would depend on their size, the Gleason grade of the tissues at the actual margins, the actual dose of radiation therapy delivered to those two separate areas of the prostate bed, etc.

    You are asking, to all intents and purposes, whether the combination of radiation therapy at 74 Gy + ADT “could have” killed any cancer cells remaining in your prostate bed as a consequence of those two positive surgical margins. The answer to that question is “Yes, it could have.” But what neither Arthur nor anyone else is going to be able to tell you is whether it actually did and has (even if we knew the specific additional information about size of margin, Gleason grade of tissue, etc.). As Arthur stated previously, the answer to that question will only become known over the next 2 years.

    Arthur would also point out that the way you are framing the question takes no account of the possibility that — quite apart from the positive surgical margins — other microscopic prostate cancer tumors too small to be visible on any type of scan may have started to grow elsewhere in your body, prior to either surgery or radiation therapy, in places which have not been radiated but have only been affected to date by the ADT (e.g., the bone marrow). The combination of perineural invasion along with your Gleason score of 9 does make that a meaningful possibility independent of the positive surgical margins.

    Arthur understands that you are seeking a high degree of certainty that the combination of radiation therapy + ADT after the prior surgery has actually cured your prostate cancer, but neither Arthur nor anyone else can tell you the answer to that question. It appears to Arthur that your clinical team has given you every reasonable possibility of a good outcome, but neither Arthur nor they can make promises about the quality of that outcome. Neither life nor medicine come with that degree of certainty.

  113. Many thanks to you dear Arthur.

    Your answer is very precise on the risk entailed by the positive margins. Now I learn from you that this risk has been dealt with the radiation treatment which is a killer unlike the ADT treatment which is a suppressor. I know there is no 100% risk elimination for cancer and thus early predictions are extremely difficult. My urologist surgeon gave me evasive answers when I asked him to explain what these positive surgical margins mean. Now I understand at least this risk factor has been added by him by not being able to remove 100% of the tumour by the prostatectomy surgery and he has left some residual cancer cells for me!

    I also appreciate that you have gone further to explain the future uncertainties regarding micrometastasis which is a common issue for aggressive prostate cancer. I did not include this aspect in my question because I was aware of the fact that in prostate cancer micro cell leakage is possible even at a very early stage when the organ-confined tumour is very small.

    I look at this major crisis in my life as a unique new learning opportunity and prepare for any battle with my slogan “Never Say Die”. Being empowered with knowledge is winning of at least 50% of the battle. The balance has to be fought bravely!

    Whenever I find any bafflements in my learning process certainly I will come to you without any hesitation for you are a great resource person with unparalleled knowledge in this subject!

    In all earnest I will accept your valuable advice and have more patience with the ongoing treatment during these early stages.

    A great deal of thanks!


  114. Dear Arthur,

    Thank you so much for your response, this Website is a godsend!

    I had one follow-up question. When a prostatectomy hasn’t been done like in my father’s case, can ADT lead to undetectable PSA levels? My understanding was that the prostate cells (not the prostate cancer cells) would still produce PSA and so PSA can’t go undetectable. Or do healthy prostate cells also die/become inactive through ADT, in which the undetectable PSA makes sense.

    Thanks so much!



    Arthur responded as follows:

    Dear Sankalp:

    Arthur says that ADT is a biochemical process designed to stop the production of testosterone and, thus, to stop the growth of prostate cells and prostate cancer cells. Without the continuing growth of prostate cells and prostate cancer cells, there can be no production of PSA, and so, “Yes”, a man’s PSA level can fall into the undetectable range (at least for a period of time) after he starts ADT — even though he still has a prostate. Ideally, you want your father’s PSA level to drop to < 0.1 ng/ml and stay there.

    However, after a while (which can be very variable from man to man, sometimes months and sometimes years) the body adjusts and finds new ways to stimulate production of testosterone, which is why the PSA will start to rise again after a period of time and the patient becomes "castrate-resistant".

  115. Dear Arthur,

    You have mentioned above that “after some time the body adjusts and finds new ways to stimulate production of testosterone” resulting in the PSA rising and making the cancer cells “castrate resistant”. Could you please throw some light on the following.

    (1) Castrate resistant means “hormone refractory” where the cancer cells don’t need androgen anymore for their activities (growth and spread being hormone independent). Then what is the use of body finding new ways to stimulate the production of testosterone? (I do not mean for the use of other body functions.) That means during such a period even without testosterone the PSA levels can go up due to the activities of the cancer cells.

    (2) When you say the body finds new ways to stimulate production of testosterone do you mean whilst the ADT is continuing the testicles are stimulated by other signals from the body contrary to the stop signal given by the LHRH agonist (ADT)? My understanding is testosterone is produced only in the testicles and some other androgen is produced in the adrenal glands. And the ADT is directed only to the testicles.

    (3) I remember having read somewhere certain cancer cells developing the ability to produce testosterone and other required substances on their own for their progression.

    I am not quite sure as to the validity of the above points since my knowledge on this subject is very limited. You are the authority who can simplify these matters and guide us to get the facts straightened.

    Many thanks to you Arthur.



    Dear Sisira:

    Arthur says that when men with prostate cancer become castrate resistant (i.e., when they no longer respond to standard forms of treatment with drugs like LHRH agonists and antiandrogens), they can do so for a range of extremely complex reasons that you can read about in articles like this one by Karatanos et al. if you really want to.

    Basically, this has nothing to do with the production of testosterone in the testicles. It has to do with the fact that other biochemical pathways in specific types of cell can be “hijacked” into producing other androgens (most specifically a biochemical called dihydrotestosterone) that stimulate the growth of the prostate cancer cells, and the production of these other androgens is not prevented by the standard forms of hormone therapy.

    Newer forms of therapy (e.g., abiraterone acetate/Zytiga and enzalutamide/Xtandi) may work for a while along with standard hormonal therapies to delay progression of “castration-resistant” prostate cancer … but in most cases they will only work effectively for a few more months. Docetaxel-based chemotherapy can also delay the progression of late-stage, castration-resistnt prostate cancer for a little while. However, …

    Arthur thinks we are getting into a great deal of detail here that is unlikely to be of any real help to your father. If you are interested scientifically in all the different the ways in which the biomedical research community has tried to prevent the progression of advanced prostate cancer over the past 30 years, Arthur would suggest you really need a specialist in prostate cancer endocrinology and pharmacology to talk to.

    From the perspective of how father can best be treated, unless your father can be enrolled into clinical trials of newer and different types of therapy (and he may or may not want to do that, because involvement in such clinical trials can come with significant risks as well as some, and maybe only small, benefits), what you really need to be focused on is the quality of his remaining life as opposed to exactly how the various types of drugs work. Hundreds of people around the world who are much smarter that Arthur have been trying to develop new drugs for the management of prostate cancer for 40+ years. We have made some progress in the past 15 years in the sense that we have found forms of chemotherapy and second-line antiandrogenic agents that can work for a while in men with castration-resistant prostate cancer. However, on average, these newer types of therapy still only extend patients’ lives by a matter of a few months, and the quality of life of most of the patients who do respond to these new drugs will already be declining quite rapidly. Furthermore, the costs associated with treatment with drugs like Zytiga and Xtandi are considerable.

  116. Dear Arthur,

    Thank you very much for your most generous efforts to elaborate the well established facts to clarify the points I presented to you. I went through your detailed explanation as well as the material you have advised me to refer in your text underlined. The bottom line I was able to grasp though not encouraging is “There is no cure for metastatic prostate cancer.”

    Best regards



    Arthur responded as follows:

    Arthur says that that is correct. There is no cure. The critical question is how long the individual patient’s cancer can be prevented from progressing, and, as I advised you earlier, that can be extremely variable because it depends on the precise nature of the individual cancer, how well the patient responds to the available types of therapy, and (we suspect) the strength of the patient’s own immune system function.

  117. I’ve been reading about the PSA bounce but haven’t found any information on how long the bounce can last. My PSA has been rising for the last four readings every 3 months. I had radiation treatment and 2 years of Eligard shots. Is it possible this could be a bounce?


    Arthur responded as follows:

    Dear Michael:

    Arthur says that it is impossible to determine whether what you are observing is a PSA bounce or not based solely on the information you have given above above.

    If you could tell Arthur all of the following information, he may be able to give you some meaningful input:

    — The dates on which you started and completed radiation therapy
    — The dates on which you had your first and your last Eligard injections and how long each Eligard injection was designed to last (e.g., 3 months or 4 months)
    — The results of your last four PSA tests and the exact dates on which blood was drawn for those PSA tests.

  118. Michael:

    Arthur says maybe you tried to leave him another message from your iPhone, but it didn’t come through at all.

  119. Dear Arthur,

    You and I have agreed on the bitter truth “There is no cure for metastatic prostate cancer”. However, please be kind enough to explain the following to me.

    1. A prostate cancer patient’s PSA rises from a non-detectable level after 2 years to 2.0 ng/ml. On investigation it was found that there was a metastatic deposit in his third lumber vertebra and there were no other metastases elsewhere in the body. (I understand this statement has its limitations.). The metastatic deposit was removed completely by radiation and the PSA goes back down to a non-detectable level and has remained so ever since. Assuming that there was only one metastatic deposit for this particular case, was it not cured by radiation. (Please do not say it is in long term remission.) Is a cure not possible under any circumstances for metastatic prostate cancer? I have read some oncologists having said “You are now cured” in like cases.

    2. Do chemotherapy drugs kill cancer cells wherever they are hidden in the body? I have seen them being used as a last resort when other therapies fail and the cancer spread becomes highly uncontrollable. Comparatively the cancer volume is small and less aggressive during early stages and easier to be eradicated rather than having to wait until the cancer volume becomes larger, aggressive, and spread to distant parts of the body. Therefore why don’t we use chemotherapy drugs when the cancer volume is small and destroy the cancer cells upfront without using other treatment protocols (first line but conventional) such as ADT which can only suppress the growth and spread of cancer but not really destroy. (Side effects may be very much less in the latter case but worth the effort for a possible eradication at the earliest stage when the cell volume is minimum.) Since chemotherapy cannot be used over long periods, is there a medical law/principle that other treatment therapies cannot be used if chemotherapy has been tried earlier?

    3. To assess the risk of recurrence for my prostate cancer after surgery I used the “Kattan nomogram”
    The following variables from my post-surgery pathology report were entered: PSA before surgery, 11.7; age at the time of surgery, 68 years; months without detectable PSA following surgery, 4; Gleason score, 4 + 5 = 9; surgical margins, positive; extracapsular extension, no; cancer in the seminal vesicles, no; cancer in the pelvic lymph nodes, no.

    The above variables are all before I received ADT and Radiation Therapy.

    The calculator gave the following risk levels for recurrence of the cancer post-surgery for my case: at 2 years, 42%; at 5 years, 68%; at 7 years, 75%; at 10 years, 82%. It also projected a probability of cancer-specific survival of 95% at 15 years.

    (a) I understand that the cancer recurrence risk in my case is high mainly because of the high Gleason score and the positive surgical margins. Could you kindly explain to me why despite this high recurrence risk the 15-year cancer specific survival for me is a very favourable 95%?

    (b) Do you think that now, since I have received radiation and being treated with ADT, the above risk gradings can change significantly in my favour?

    Thank you very much in advance.

    Best regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur has offered answers to your questions using the same numbering system.

    (1) Arthur says that it is possible, but extremely rare, for men like the one you describe to be cured of metastatic prostate cancer. However, any doctor who declared a man to be “cured” under such circumstances would probably have wanted to see hat patient remain in a biochemical recurrence-free state for a minimum of 5 years after the combination of radiation + ADT before suggesting that he might be cured. A man who was biochemical recurrence-free for less than 5 years is one that Arthur would only describe as being in long-term remission, and such men have been known to have recurrent disease 5, 10, or 15 years after the second-line therapy. A true “cure” can only have been said to have occurred if a man never has a recurrence. You also need to understand that you are making all sorts of assumptions about the case that you describe that are probably unprovable.

    (2) The use of chemotherapy early on in cases such as the one you describe is certainly possible, but, when it is done it is usually done in combination with ADT, not as chemotherapy alone. However, it has never been proven that such early use of chemotherapy is effective in the elimination of the cancer because it would take something like 15+ years to follow such patients for long enough to establish a survival benefit. Arthur is aware of a number of young patients initially diagnosed with high-risk disease but non-metastatic disease who were treated with surgery, radiation therapy, ADT, and chemotherapy to make every attempt to eliminate their cancer. This strategy appears to have worked for some of them and certainly didn’t work for others. Effective forms of chemotherapy can not, necessarily “kill cancer cells wherever they are hidden in the body”. If they could, we would simply treat all men with chemotherapy up front, but chemotherapy really isn’t that effective. Usually the best we get out of chemotherapy is assistance in placing a man back into remission … but there are rare exceptions.

    (3) Arthur says that when he re-ran the post-surgical nomogram you used to assess your risk for recurrence after your PSA started to rise again, using exactly the data that you provided above, he got a slightly different set of results to the ones that you say you got. The results Arthur got (based on PSA before surgery, 11.7; age at the time of surgery, 68 years; months without detectable PSA following surgery, 4; Gleason score, 4 + 5 = 9; surgical margins, positive; extracapsular extension, no; cancer in the seminal vesicles, no; cancer in the pelvic lymph nodes, no) were

    Probability of recurrence of the cancer post-surgery: at 2 years, 39%; at 5 years, 64%; at 7 years, 72%; at 10 years, 79%. It also projected a probability of cancer-specific survival of 95% at 15 years.

    However, the real question, after it was determined that you needed salvage radiation + ADT, would be what the salvage radiation therapy nomogram projected. Once a cancer has recurred, the original projections of the earlier post-surgical nomogram become irrelevant.

    With regard to your other question, most men whose PSA drops to undetectable after first-line surgery have a relatively good chance of living for 15 years so long as they don’t have multiple adverse factors (e.g., Gleason 9 disease and positive surgical margins, and positive seminal vesicles and positive lymph nodes). A man with these four risk factors would be considered to be at very high risk for progression as opposed to just high risk. Of course the presumption that they will live for another 15 years is based on the idea that they would respond relatively normally to long-term ADT and other therapies.

    Because you had a metastatic recurrence of your cancer originally (as opposed to a local recurrence), you also have to appreciate that your risk for another metastatic recurrence is significantly higher than that of a man whose initial recurrence requiring salvage radiation therapy was a local recurrence.

    You need to appreciate that Arthur cannot tell you what will happen to you … and in truth neither can anyone else. You might live for another 20 years … or your PSA might start to rise rapidly tomorrow because there is a tiny focus of metastatic disease hidden deep in your bone marrow (and it could have been there by the time you were originally diagnosed). All this analysis will not change that.

    If you want to have chemotherapy now in the hope that it might decrease your risk for recurrence of your cancer, you need to talk to your doctor about that. Might it work? Yes it might. Can you be sure it would work? No, you can’t. Can anyone give you such an assurance that any form of treatment would eliminate any cancer left in your body (if there is any)? No, they can’t.

  120. Dear Arthur,

    Your answers only stunned me for their absolute clarity and completeness! Its a great deal of information for me.

    In the second paragraph before the last, you have mentioned “Because you had metastatic recurrence of your cancer originally …”

    I would like to know what made you identify this situation in my case (a metastatic recurrence originally).

    I owe you a Big Thank You.

    Best regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur had a lot on his plate yesterday. He confused the case you presented in question (1) of your prior question with your own case, which was why he thought you had had a metastatic recurrence.

  121. Dear Arthur,

    About the confusion, I thought as much.

    Thank you very much for sending me the correct risk gradings using the nomogram. I too rechecked and found the same figures. The risk has decreased slightly in my favour.

    You have expressed two views to my related question on the 15-year prostate cancer specific survival (95% in my case):

    (a) “… most men whose PSA drops to undetectable after first-line surgery have a relatively good chance of living for 15 years so long as they don’t have multiple adverse factors (e.g., Gleason 9 disease and positive surgical margins, and positive seminal vesicles and positive lymph nodes). “.

    I wonder whether this pre-qualification is needed since the nomogram calculation has taken into account all these high-risk factors as well. For my own case I entered “positive” (“Yes”) to these last four variables in the nomogram and then the 15-year cancer specific survival changed to 63% (a significant change from 95%). That means the final survival grading has taken into consideration all risk factors.

    (b) “Of course the presumption that they will live for another 15 years is based on the idea that they would respond relatively normally to long-term ADT and other therapies”. This I think is more acceptable. If there is any doubt, I will only be too glad to take the “benefit of the doubt” to myself!

    Many thanks once again


  122. Dear Arthur,

    In the light of my above interpretation do you like to clarify further why the nomogram gives 95% for 15-year survival as against a high risk rating for cancer recurrence in my actual case (irrespective of what you have stated as … “so long as they don’t have multiple adverse factors …)?

    I feel it needs further thinking because the 15-year survival rate has changed to 63% when I added more negative variables (hypothetical but all adverse factors you have spoken of included).

    I am sure you will hit it on the head this time.

    Thanks and regards



    Arthur responded as follows:

    Dear Sisira:

    The Kattan nomograms are simply predictive tools based on data from thousands of other patients over time. Arthur is in no position to be able to explain “why” the data for a particular patient give a particular result. All that he can tell you is that the vast majority of men will live for at least 15 years after a diagnosis of localized prostate cancer. If you had been diagnosed with metastatic prostate cancer, it would be a different story, but given your diagnosis the projection of 95% probability of 15-year survival (or longer) is not exactly surprising.

  123. Dear Arthur,

    Quite apart from a medical view point, your words give me great consolation because my hidden desire was to learn from somebody who is authoritative that I can live that long at least thanks to the nomogram! There is no substitute for a hope.

    Thank you for your unique kindness of answering questions from all angles. It indeed is a rare quality and also a rare ability.

    Best regards.


  124. Dear Arthur,

    I am still on my 3rd Zoladex and my 4th one is due on 24 January 2016. My last PSA test reading was 0.003ng/ml. This was after RRP and EBRT. I reported my case in detail to you on 2.11.2015 and since have received your valuable answers to many questions I sent to you for which I say a big thank you once again.

    I joined YANA prostate cancer support group site in April this year and have posted my case with the updates under my name Sisira Ramanayake from Srin Lanka. I am the only one from my country and also from the whole of Asia who have joined YANA, a site immensely useful to prostate cancer patients. I went through about 1000 survivor stories posted in the site and selected for printing hard copies of the cases which show similar pathological conditions compared with mine. Specially Gleason 9 and 10 cases as well as few Gleason 8 cases. All are receiving treatment and surviving as of today. They have all agreed to be YANA – Mentors and given their e-mail addresses and I have already started communicating with many of them. We learn a lot from each other’s experience.

    One thing I have observed from many prostate cancer patients is that they have a harder battle with their Doctors than with the Cancer itself because of their attitudes. My own experience with the Urologists and Oncologists too is no different. But I am learning fast to “hold the bulls by their horns” and get the justice done without offending them by educating myself as much as possible on this subject. The firsthand information I receive from YANA and “Arthur’s Torch of Education” that never fails give me such empowerment that makes me so fearless. I also observe few YANA story tellers are in high praise for their Urologists/Oncologists for the great concern they show and the efforts taken to heal them and save their lives despite the fact that cancer is a terminal illness. Dr.Charles Myers from Virginia and Dr.Patric C. Walsh from John Hopkins Hospital are two such names I have learned. The difference I notice is that they have a wholistic approach in treating the cancer patient. While treating with the cancer drugs they advise on proper food supplements, vitamins, exercises and maintaining the balance of other metabolic functions.

    My doctors have not spoken to me anything regarding the above but have given me the right and the best first line treatment for the cancer. But I want to be proactive in my own interest because there is a long way to go. Now I want to ask two questions from you.

    1. I have seen in several YANA cases that they take supplements such as Pomegranate, Broccoli, Green Tea and Turmeric ( curcumin ). I saw in the internet a product called Pomi – T ( capsules ) containing these four food elements in concentrated form. Are these capsules reliable?
    Green Tea of course I drink daily. For the other three it will be easier if I can take capsules. What is your advice? Do you know reliable other names of similar pills?

    2. Oncologists advise their patients to avoid red meat,eggs and dairy products. Is it because they increase bad cholesterol and affect cardiac problems or such food promote cancer progression quite apart from cardiac issues?
    For years I have been eating vegetables and fish only but I eat three eggs for a week. Should I omit eggs? I have no cholesterol or cardiac issues whatsoever.

    Peace, Happiness and Good Health to you Arthur!



    Arthur responded as follows:

    Dear Sisira:

    Men in the Western world tend to have much less healthy diets (and they eat much more) than men in nations like Sri Lanka, where diets are much more often very low in meat and carbohydrates and much higher in things like fish and vegetables. So your current diet is probably much more healthy in any case than most of the Caucasian males whose data can be found on the YANA web site.

    The relative value of supplements like pomegranate, broccoli, turmeric — let alone Pomi-T capsules — has to be seen in that context.

    In all honesty, Arthur says we have no good data at all to suggest that use of supplements like Pomi-T are of any clinical benefit at all. The only really good and available evidence is that they can have short-term effects on some men’s PSA levels and this can make some men “feel better”; and they certainly don’t come with any significant, known side effects. In your particular case, however, because you already have a very “heart healthy” lifestyle, Arthur sees no particular need for you to be considering use of any of these products. In addition, since your PSA is already about as low as it can get, using products like Pomi-T or other supplements aren’t going to have any impact on your PSA.

    With respect to the eggs, Arthur says there is a lot of noise (but very little really good evidence) about how many eggs may or may not be “good” for one, but that too has to be taken in the context of the rest of any man’s diet. Your diet, by Western standards, is relatively low in protein. Thus, Arthur’s opinion would be that reducing your egg intake from three eggs to one egg a week might actually be bad for you rather than good. If you were normally eating two eggs a day and also had a significant amount of red meat and other dairy products in your diet, the situation would be different … but you don’t, so Arthur thinks you should just stick to what you have been doing (subject to any views your doctors may have expressed on this topic).

  125. Dear Arthur,

    Thank you very much for sending me your reply in no time. Your valuable advice is quite acceptable as usual.

    Would you be kind enough to further clarify the following:

    1. As indicated in my second question, the impact of certain food on prostate cancer growth and spread. I can understand very well when a cardiologist advises to avoid eating red meat, dairy products and eggs to prevent coronary issues. But when the same advice comes from the oncologist I do not understand what his concerns are. That is why I am asking you this question whether these food items have any significant impact n the growth and progression of prostate cancer cells. “Heart healthy food” is not the issue.

    2. Your explanation is very clear on the use of Pomi – T capsules in my specific situation. I quite often eat Pomegranate fresh fruits, include Broccoli in our vegetable soups and also add Turmeric to our daily curries. So I think that is more than enough rather than going for a standardised capsule. Thanks for your advice.


    Arthur responded as follows:

    Dear Sisira:

    Arthur says that unless your oncologist has specifically advised you that you need to cut down on your egg consumption, Arthur knows of no compelling evidence whatsoever to suggest that a man with prostate cancer but good cardiovascular function and a normal cholesterol level who is eating three eggs a week needs to cut back on his egg consumption.

    You did not tell Arthur that your oncologist had given you such advice — only that you had read this somewhere. Arthur would need to be able to know exactly where you had read this to be able to tell you why this did or didn’t apply to you … but, as Arthur has now told you twice, he knows of no good reason why it would apply to you.

  126. Dear Arthur,

    I am sorry to say this time that you have misinterpreted my question. The question is not about “eggs are good or not good for me”. This you have sorted out for me.What I am specifically asking is whether food items such as red meat, dairy products and eggs when consumed more will contribute to the growth and progression of prostate cancer cells of a person diagnosed for prostate carcinoma. Their growth promoters are only androgenic substances and the like other chemicals, which I do not really know.

    If this question has no sense, please ignore it as you may get irritated over my questions, having to say “why not ask your Oncologist”.

    Thank you for your time and patience.



    Dear Sisira:

    Arthur says that, like most questions about diet and risk for getting cancer or having progressive cancer, we really don’t know if there is a cause and effect relationship. There is certainly an association between risk for progressive disease and a diet high in red meat, dairy products, and eggs, but whether eating high quantities of red meat, dairy products, and eggs actually causes progression is unknown.

  127. I think there are epidemiologic/population based studies that surmise, outside of clinical study, that cultural diets have fewer rates of cancer in select populations. UCSF and other cancer research centers are underway with long-term, clinical studies and lesser forms of research on the diets of tomatoes, reduced fats, vegetable-based proteins, cardiovascular exercise, and avoidance of red meats, treated meats, etc.


    Arthur responded as follows:

    Dear gmac53:

    Arthur says that these types of study add to the “association” information, but they still can’t tell us about cause and effect.

  128. Dear Arthur:

    May I most humbly tell you that I have no intention whatsoever to contest your views. But it appears that these food items in question are “known” to promote prostate cancer growth when consumed in excess. As you have rightly pointed out nobody has told us the “cause and effect link”. That was exactly what I was trying to find out from you as a matter of interest. The link is very clear in the case of the cardiac issue, that these foods increase bad cholesterol and triglycerides blocking the blood vessels.

    Additionally, after having read your previous reply and your desire to know where I had exactly read such information, recalling several such instances I resorted to Google with the hope of finding a definite and clear source to tell you this is exactly what I mean.

    I quote below from the “WebMD”

    Main topic : Is there a Prostate Cancer Diet?

    Sub topic : Nutritional Recommendations (Items ranging from 1 to 18)

    No.1 says “Reduce animal fat in your diet. Studies show that excess fat, primarily red meat and high fat diary, stimulate prostate cancer to grow”.

    No.2 says “Avoid trans fatty acids which are known to promate cancer growth. They are high in margarine, and fried and baked foods”.

    No.5 says “Avoid high calcium diets, which have been shown to stimulate prostate cancer growth”.

    I think it is reasonable for me to interpret “stimulate prostate cancer growth” as a significant impact on disease progression.

    However, in the absence of a sound linkage let us settle down to “heart healthy food” is “prostate healthy” too.

    Many thanks for your time.


  129. Dear Arthur,

    I am a 43-year-old male recently diagnosed with 3 + 4 Gleason score prostate cancer. I am still researching the disease and options but my diagnosing MD feels strongly that prostatectomy is the right approach. All the literature indicates that the quality of the surgeon affects the results of the procedure. Are there list or guides of the top surgeons in the country or by region? Thanks for any input you have.


    Arthur responded as follows:

    Dear Rybuild:

    Arthur is not aware of any truly meaningful lists of “the best” prostate cancer surgeons in the USA. And you also need to appreciate that a urologist is almost certainly going to tell you that radical prostatectomy is the most appropriate form of treatment for someone like you, but … Arthur says it is really important that you appreciate the potential side effects and complications of surgical treatment (see this recent article) and the full range of your options today.

    Arthur says that if you join our social network, it is specifically designed to help you think through all of your options. When you sign up, it helps if you state your age, your clinical stage, your Gleason score (4 + 3), the total number of biopsy cores taken at biopsy, the number of those cores that were positive for cancer, and anything else you can think of that might be useful.

    Just to give you an example, Arthur says that if you have only one small focus of Gleason 3 + 4 = 7 cancer, you might be a good candidate for focal therapy (like a lumpectomy for breast cancer) at one of the small number of centers that specialize in exploring this technique … and then you might be left with a functional prostate, and a far higher quality of life than if you had a radical prostatectomy!

  130. Hi Arthur,

    In August 2014 I had a TURP operation to reduce the size of my prostate, which was putting pressure on my bladder, causing me urinary problems that were not being alleviated by a combination of Flomax and Avodart.

    The operation went fine. I recovered quickly and my urinary problems improved greatly. During the operation a sample of prostate tissue (transurethral resection) was removed for biopsy. The biopsy result indicated that I had focal adenocarcinoma with a Gleason score of 5 (3 + 2) involving 1% of tissue. My urologist (the one who performed the TURP) and my primary care physician (an internist) are both of the opinion that my situation is simply a precancerous situation. Both feel that monitoring my PSA every 6 months is the best strategy at present to follow. My total PSA results* from November 2011 to November 2015 are:

    11/25/2011 = 1.0
    11/27/2013 = 1.4
    11/21/14 = 1.7
    5/28/15 = 2.3
    11/19/15 = 3.0

    I am presently 76 years old and am in good health. As you can see, over the last four years my PSA has risen from 1.0 to 3.0, which of course is still less than 4.0.

    I understand you are not a physician. And it is not my intent to push the Panic Button given my diagnosis. However, I would appreciate if you could comment as to your take on my physicians’ strategy. Both think a Gleason score of 5 is very low and is essentially a precancerous condition.


    John Bonner, PhD (in history)

    * All PSA results determined by the Siemens chemiluminescent method


    Arthur responded as follows:

    Dear John:

    Arthur says that your data certainly appear to suggest that you have a form of low- or very low-risk (indolent or near to indolent) prostate cancer which can simply be monitored for a significant period of time (and potentially for the rest of your life) without any need for invasive treatment.

    It is clear that you have benign prostatic hyperplasia (BPH), and so this could easily account for the continued rise in your PSA level since the TURP, and any form of invasive treatment at your age comes with a degree of risk to your quality of life in terms of urinary function (and perhaps erectile/sexual function too) that you would probably prefer to avoid.

    Arthur also says that, to get a greater degree of confidence about the long-term effectiveness of simple monitoring as a way to manage low-risk prostate cancer like this, you might want to read this relatively recent commentary on a paper from the group at Johns Hopkins, who have been following well over 1,000 men with low-risk prostate cancer initially monitored on active surveillance. As you will see, the actuarial probabilities of prostate cancer-specific survival and metastasis-free survival for the men in this group at 10 and 15 years were all > 99%.

    If your PSA continues to rise, then at some point you might want to talk to your doctors about the value of a multiparametric MRI of the prostate to see if there is any sign of more extensive prostate cancer that might need to be rebiopsied to see if it has a higher Gleason score than 6, but on the principle of “first do no harm” Arthur thinks that the guidance you are getting from your doctors appears to be very sound indeed.

  131. My original plan (before I asked you) was to do exactly what you suggest. Namely, just monitor it via PSA testing twice a year. And after reading your advice, I intend to stick to this plan unless something more serious arises (such as more rapidly rising PSA levels) that warrants a more aggressive approach. I’ve never heard of multiparametric MRI of the prostate and will keep this in mind should I have to take a more aggressive approach.

    Thank you for your advice. I appreciate your quick reply.


  132. Arthur:

    I would appreciate your input regarding the following information. My family doctor, because of a rise in my PSA, referred me to a urologist. My PSA was 4.2 at the time. After the usual DRE (my prostate being normal) and discussion he advised he would like to do a biopsy. My age at that time was 74; the year 2010. The results of the biopsy, which took a total of 12 cores, was 11 totally free of cancer; however, the 12th core indicated cancer but in less then 5 percent.

    We agreed to an active surveillance (AS) program with another biopsy in 1 year. I was placed on finasterde to shrink the prostate for a better biopsy. In 2011 I had another 12-core biopsy with all 12 cores free of any cancer. I am now 80 years old and in excellent health. With my urologist’s OK, I stopped the use of the finasteride because of the side effects. My PSA at that time was 6.3. On my follow-up visit in November 2015 my PSA had risen to 8.3 after being off the finasteride for 6 months. However, the DRE indicated a nodule on the right side of the prostate. My urologist indicated he would like to do an ultrasound the following week. The results on the film showed an area about the size of a dime and very white in color. The overall condition of the prostate was excellent. His remark was he didn’t feel there was cancer and we set a follow up visit for February 2016 to see if my PSA had spiked. I am sort of uneasy about my return visit, should my PSA increase, and the direction I should take at this time.

    Thank you for any input you may have after reading the facts.


    Arthur responded as follows:

    Dear William:

    Arthur would suggest that you have three possible options for the immediate future, as follows:

    (1) Do nothing until you know the results of your next PSA test in February and then talk to the doctor about
    (2) Just staying on AS
    (3) Having a multiparametric MRI (if you can get such an imaging test through your urologist or at another facility near to where you live)
    (4) Ask about having another biopsy, with samples being taken specifically of the white area.

    Arthur is unable to tell you what the “white area” might signify. He is not a doctor, let alone a specialist in reading ultrasound scans.

    You could, of course, ask your urologist what he thinks the “white area” shows if he is confident that it is not prostate cancer.

    At 80 years of age, after having been diagnosed with a low-risk prostate cancer back in 2010 and with a PSA that rose to 8.3 ng/ml after being taken off several years of finasteride therapy, it seems highly unlikely to Arthur that you now have an aggressive prostate cancer that could lead to your death (based on the information that you have provided). Is it a possibility? Well, yes, it is a possibility! And it is also a possibility that you could be killed by a falling asteroid 3 years from now. However, it was completely ;predictable that your PSA was likely to rise after you cam off the finasteride.

    Arthur says that the question you really need to think about is this one. What would you really want to do if your PSA actually rose to (say) 10 ng/ml by May 1, 2016? And a repeat biopsy showed a small amount of Gleason 3 + 4 = 7 prostate cancer in one of 11 cores. The latest NCCN guidelines suggest that active surveillance would remain a perfectly reasonable form of management in such a case. Surgery in 80-year-olds is rarely recommended because of the high-risk for problems with post-surgical continence. And there is no evidence whatsoever that any form of immediate treatment would be likely to extend your overall survival.

    Now Arthur does understand your angst about the rising PSA and the white area on the TRUS scan. One other thing you could do would be to go to get a second opinion from someone who specializes in early stage prostate cancer at a major academic prostate cancer. You might feel more comfortable if a specialist like that gave you the same guidance that you are getting from your current urologist. What Arthur can also tell you, however, is that the guidance you are currently getting makes perfect sense to him, given the facts. If your PSA continues to rise, some sort of action may be necessary, but it might be as bland as going back onto the finasteride (or trying another similar drug called dutasteride instead).

  133. Dear Arthur,

    After my radical prostatectomy in March and adjuvant radiation treatment to the prostate bed during July-August last year, I have been on double blockade ADT with Zoladex 10.8 mg and Calutide 50 mg once daily, commencing in April 2015. My cancer was T2cN0Mx, Gleason 4 + 5 = 9 and details of my pathology report were given in my original posting on this web site dated November 2, 2015, which you may refer if necessary. I used to check my PSA every 3 months just before taking the Zoladex injection. My fourth Zoladex shot is due on 27 January 2016 and on this date I will be meeting my Urologist to review the position after taking the injection.

    I am little worried about my last PSA test reading dated 20.1.2016, which is 0.008 ng/ml, because it shows a noticeable increase from the previous one and also from the lowest recorded it shows an increasing trend. I give below the values of the PSA tests done from the same lab.

    20.1.2016 — 0.008ng/ml
    19.10.2015 — 0.003ng/ml
    15. 8 2015 — 0.001ng/ml
    6. 6.2015 — 0.002ng/ml

    Before RRP my PSA levels were: 5.11, 6.88, 7.50, 11.70 ng/ml.

    Please give your valuable opinion regarding my following questions:

    1. Does this PSA trend with the last increased value suggest a biochemical relapse and an early recurrence of the cancer despite the treatments given?

    2. Since I have undergone prostatectomy, at what point of PSA value stability should be achieved to continue without worrying about a relapse and what should be the safest undetectable cut-off point?

    3. At this level of PSA. is it too early to calculate the PSA doubling time to get an idea as to how soon the cancer will come back? (I used a nomogram and and did the calculation using the available PSA values — post RP — and got the doubling time as 3.03 months (0.25 years ). Velocity = 0 ng/mL/month. I have learned that the longer the doubling time the more favourable it is prognostically and shorter times indicate the aggressiveness of the cancer progression.)

    4. After taking my fourth Zoladex shot this time, I thought of taking a holiday and thereafter continuing with intermittent hormone therapy — 1 year on and 2 years off (3-year cycles) if this approach fits me because same is considered as a more strategic treatment approach with the anticipated benefit of pushing away the event of prostate cancer cells developing resistance to hormone therapy and become hormone refractory. Do you think I can go for this ADT style right now taking the holiday from 27 April 2016 irrespective of the present status of my PSA values? With your valuable inputs, I should be able to discuss with my urologist about the appropriate strategy.

    Your opinions and guidelines would be greatly appreciated.

    Best regards,



    Arthur responded as follows:

    Dear Sisira:

    Re Q1: No. Arthur says the rise in your PSA to 0.008 ng/ml does not necessarily indicate a biochemical relapse … but if your PSA rises again (say to 0.015 ng/ml) at your next PSA test in April, then the likelihood of biochemical relapse is high.

    Re Q2: Arthur says there is no specific PSA cut-point at which a patient can know he is unlikely to relapse. Safety from biochemical relapse is dependent on a stable PSA level over time, and the lower the PSA level the better.

    Re Q3: Arthur says that yes, it is too early for you to be using these data to accurately estimate PSA dioubling times based on ultrasensitive PSA levels. PSA doubling times have only been accurately validated for men with PSA values of 0.1 ng/ml and higher.

    Re Q4: Arthur says that if your PSA level was to drop back down again from 0.008 to 0.003 ng/ml at the time of your next PSA test (at the end of April), you could certainly discuss starting intermittent ADT with the doctors after another stable PSA of about 0.003 ng/ml at the end of July 2016. Considering intermittent ADT on the basis of your current PSA results is probably not wise. Also, you should not determine in advance how long to stay off and on ADT; a better strategy is to decide with your doctors what your PSA level would need to reach while off ADT that would suggest you needed to re-start the ADT (e.g., perhaps 5 ng/ml in a case like yours).

  134. Dear Arthur,

    Thank you very much for your prompt reply. I will act according to your advice.


  135. Hi. I am age 69 and I have been on hormone treatment (Zoladex) for prostate cancer but that no longer seems to be working. I am now advised to enter chemo, and also I can also enter one of the clinical trials ongoing, i.e., SAPROCAN or VIABLE. I wonder if anybody has any experience or knowledge of these trials to help me make up my mind.

    Up to now the cancer treatment has had no effect on my life, which tied in with a key objective of maintain my quality of life. Obviously now chemo will change things which is a bit galling, particularly as I feel fine and sometimes wonder what is going on.

    Any comments would be appreciated.




    Arthur responded as follows:

    Dear John:

    Unfortunately, making decisions about what to do next in men like you with a rising PSA after long-term and relatively successful treatment on an LHRH agonist like Zoladex has become very complicated today. It used to be easy because one had very little choice!

    So here are the options that Arthur thinks might be available to you, and you will need to discuss at least some of these options with your doctors before you can come to any decisions:

    — Just adding bicalutamide (Casodex) to your Zoladex, which might work for a few months, but won’t work for much more than that
    — Just adding enzalutamide (Xtandi) to your Zoladex — if this is a covered option under the NHS in the UK, which Arthur isn’t sure about
    — Just adding abiraterone acetate (Zytiga) to your Zoladex — again, if this is a covered option under the NHS
    — Enrolling in the VIABLE trial, which is arguably a “no lose” option because you’ll get chemotherapy either way and the side effects of dendritic cell therapy are usually relatively minor if you get randomized to that therapy

    Arthur is less enthused by the idea of the SAPROCAN trial for the simple reason that several other drugs of this type (i.e., like saracatinib/AZD0530) have been tried in the treatment of advanced prostate cancer over the years and have generally showed minimal clinical benefit but a noticeable risk for side effects. However, one never knows what might happen with a new drug and it is not a drug Arthur knows a lot about yet.

    The one thing that Arthur would want you to understand is that although docetaxel-based chemotherapy does come with risks for side effects, in general the risks associated with docetaxel-based chemotherapy are a lot less severe than those associated with older forms of chemotherapy, and many men find that they can handle treatment without really significant consequences. Arthur would encourage you to discuss with your doctors what sorts of side effects they think are likely as opposed to just what side effects are “possible”. You should also ask the doctors (or better still the study nurse) what types of “preventive care” can be taken to avoid certain type of side effect (like minimizing risk for peripheral neuropathy by keeping one’s hands and feet in ice water while receiving the chemo).

  136. Very, very informative Arthur. Thank you for always giving people such great advice.

  137. Hi.

    My husband was diagnosed in 2012 with grade 9 cancer. He had a TURP in May followed by 19 rounds of radiotherapy in August followed by Zoladex for 2 years .

    His PSA after stopping the Zoladex was initially 0.025; then 6 months later it was still 0.025; now the latest PSA level is 1.2.

    Is this anything to worry about?


    Arthur responded as follows:

    Dear Tricia:

    Arthur has to tell you that unfortunately yes, this almost certainly is something that you and your husband are going to have to worry about. And the first thing you need to talk to the doctors about is getting a repeat PSA test in about a month’s time to confirm that this rise in your husband’s PSA is “real”.

    Arthur says that if your husband’s PSA is rising like this, then at some point he is probably going to have to go back onto the Zoladex and he may want to talk to the doctors about combination therapy with Zoladex and docetaxel-based chemotherapy to try to put the cancer back into remission. We don’t yet know how effective this is in men like your husband, but we do know it can work well in men with much more advanced forms of progressive prostate cancer.

  138. Dear Arthur,

    My last posting was on January 23, 2016.

    The majority of urologists and oncologists don’t seem to attach sufficient importance to the food and vitamins once they start their treatment for a diagnosed cancer and they hardly tell anything about this subject to their cancer patients. But it is a well established fact that some foods we eat on a daily basis have a serious impact on developing diabetes, cardiovascular disease, various cancers, etc. If there are foods which can induce the growth and progression of prostate cancer, there should also be some other foods which can do the opposite.

    A well-known oncologist from the USA, in his treatment strategy for prostate cancer, highly advocates that with the main protocols such as ADT and EBRT, certain food supplements and vitamins have to be taken, which will hinder the growth and progression of the cancer cells and help the main drugs to work more effectively. The same doctor has recommended the following supplements and vitamins for cases similar to mine. His main strategy is to get the patient to a position of complete remission and the approach appears to be successful from many cases I have read.

    The recommended list:

    — Lycopene 10 mg with each meal
    — Fish oil 4000 mg a day
    — Soy isoflavones 200 mg a day
    — Vitamin D3 4000 IU a day
    — Selenium 200 mcgs a day
    — Vitamin E 200 IU a day

    As a matter of practice I do not take anything without asking my doctors first. I have read somewhere that higher doses of fish oil though Omega3 can cause a lot of gastrointestinal problems. And similarly selenium and vitamin E can fuel prostate cancer progression. Vitamin D3 is no doubt quite beneficial and I have read nothing against lycopene and soy isoflavones. Anyway I have a desire to further strengthen my present ADT therapy if the additions can yield some benefits.

    I would appreciate your comments and advice.



    Arthur responded as follows:

    Dear Sisira:

    Arthur says that here is no doubt that the use (or non-use) of dietary factors and dietary supplements can affect prostate cancer progression (and remission) in some patients. However, the degree of value of the supplements is dubious in the extreme when considered as a general rule.

    Arthur thinks that unless patients have evidence of abnormally low levels of things like vitamins (e.g., vitamin D), then taking vitamin supplements is unlikely to be of any major assistance in the management of their cancer — but there are going to be exceptions to that general rule because there is vast variation in the biology of individual humans.

    In general Arthur believes that what is important is not this supplement or that supplement — it is having a healthy, Mediterranean-type diet that is relatively low in red meat, animal fats, carbohydrates, and dairy products and relatively high in fish, fruits, vegetables, and nuts. For most patients, a diet of this type will generally provide many of the dietary supplements that are recommended by some clinicians (including the one you are referring to).

  139. Dear Arthur,

    You and I have previously discussed at length about the importance of taking a Mediterranean type of diet, avoiding red meat, dairy products, etc. And also the pros and cons of capsules containing pomegranate, broccoli, green tea, and turmeric.

    Your above answer does not satisfy my question pointing to a list of specific items. These items indicate much higher doses that you don’t find in the daily consumed food in whatever style. (e.g., fish oil 4,000 IU, selenium 200 mg, etc).

    What I wanted to know is whether you personally can agree with such a list as beneficial for prostate cancer treatment, to the best of your knowledge?

    Anyway Arthur, thank you very much for being so kind to have sent a quick reply.

    Best regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur wouldn’t personally do any of these things if he was diagnosed with prostate cancer … and he is not aware of any Level 1 data supporting any of these behaviors on a clinical basis.

  140. Dear Arthur,

    It is true that you may not do anything personally if you are diagnosed with prostate cancer! That is about the best if one can afford to do depending on the status of the cancer ( I have omitted “any of these things” and used anything personally). But this famous oncologist I have mentioned, specialising in prostate cancer treatment, himself is a prostate cancer survivor. I thought there should be some meaning to his list of recommendation in addition to the main cancer treatment and Mediterranean diet. However, I can agree with you on the lack of strong support by way of confirmed clinical trials and the division of specialists which is often prevalent in such matters.

    It is due to this blurring I was compelled to consult your opinion under such circumstances and not for the mere sake of worrying over trivial matters. Does it sound like “Can we cure prostate cancer with Fish Oil?”

    Thank you for your time and patience.

  141. Dear Sisira:

    Arthur says that being “famous” doesn’t make people right. And no, there is no way we can cure prostate cancer with things like fish oil. The best that any of these supplements may do for some people is improve aspects of their general health.

  142. Thanks a lot Arthur.

    I got your point.

    You will not be surprised to get a question next on “snake oil”!


  143. Hi Arthur,

    According to a randomized Finnish trial, as I read it, 5-alpha-reductase inhibitors might be promoting cancer in already treated men that have prostate cancer. Do you know anything about this trial and what is your opinion about it.


    Arthur responded as follows:

    Dear David:

    Arthur assumes that you are referring to this report by Murtola et al., based on data from the Finnish Prostate Cancer Screening Trial.

    It is Arthur’s belief that what this study actually tells us is the following:

    — The follow-up averaged only 7.5 years after diagnosis, which is not a long time for a group of prostate cancer patients.
    — 617/6,537 men who were diagnosed with prostate cancer (9.4%) actually died of prostate cancer; another 1,861 (28.5%) died of something else; 4,057 (62.1%) were still alive.
    — Risk of prostate cancer-specific death did not differ between the users and the non-users of 5-ARIs for use before and after diagnosis with prostate cancer.
    — Risk of prostate cancer-specific death increasedbetween the users and the non-users of alpha-blockers for use before and after diagnosis with prostate cancer.
    — The use of 5-ARIs did not appear to affect prostate cancer mortality when used in management of benign prostatic hyperplasia.

    Arthur would note, however, that the Finnish screening trial was never designed to evaluate the risk of prostate cancer in men who were or were not taking either a 5-ARI or an alpha-blocker either before or after diagnosis with prostate cancer, and so any conclusion that is drawn from this trial has to be evaluated with a great deal of caution.

    Arthur would also note that he has only been able to see the abstract of this paper and not the full text.

  144. Dear Arthur,

    This is all utterly disappointing — what 5-alpha reductase inhibitors can do! (Certainly not your fault.)

    We believe in western medical practice thinking their findings are based on hard scientific facts. But apparently it is no better than astrology! In my horoscope the starting lines would say my time is very bad and it will end up by saying my time is very good. Finally whether it is good or bad will be decided by what really happens to me!

    At present I am on double androgen blockade since my prostatectomy and IMRT. If my PSA, which is now at 0.008 ng/ml, is going to show any increase even slightly, I thought of discussing the position with my urologist and if he has no objection, go for the Triple Blockade. That means adding Avodart which is a 5-alpha-reductase inhibitor. The scientific explanation I have learned is that 5-alpha-reductase enzyme converts free testosterone to dihydrotestosterone (DHT) which is about 10 times more potent than normal testosterone and such conversion of even a small amount to DHT can fuel the growth of prostate cancer cells. The inhibitor can therefore stop this process and make the androgen deprivation therapy more effective.

    Now I am really confused! Science or fiction?

    What should I do?

    Best regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur says that you appear to be confusing science with medicine.

    Scientifically, it is correct that the progression of prostate cancer is fueled (in large part, but not exclusively) by the conversion of testosterone to DHT through the activities of enzymes known as 5-alpha-reductases. Scientifically, it is also correct that a 5-alpha-reductase inhibitor (5-ARI) can — to some extent — block the ability of the enzyme to facilitate that conversion. However, … medically the effectiveness of 5-ARIs in blocking the actions of the 5-alpha-reductase enzymes can vary significantly from patient to patient.

    What we do not have is any really definitive medical evidence that adding a 5-ARI to standard forms of combined androgen deprivation (e.g., an LHRH agonist + an antiandrogen) makes any clinical difference to either the progression-free survival or the overall survival of the majority of men with advanced forms of prostate cancer.

    Arthur would note simply that just because one can demonstrate something in a laboratory or in animal models, or even in small numbers of humans, does not mean that it necessarily going to work clinically for most patients. There is a difference between science and medicine.

    Having said that, Arthur would note that, on a case study basis, there certainly do appear to be men whose cancer progression can be significantly affected by the use of triple androgen blockade. Whether you are one of those men, no one can tell you in advance at this time. Furthermore, we have no really clear idea why this clinical effect appears to be positive in some men and not in others. Arthur’s personal suspicion is that this may have something to do with the individual nature of the immunobiological status of these patients together with the genetic/genomic characteristics of their particular form of prostate cancer. Please remember that prostate cancer is far from being one specific disease. We have known for a while now that there are multiple subtypes of adenocarcinoma of the prostate. It would not be surprising to find that some of these responded better than other to triple androgen blockade.

  145. Dear Arthur,

    Your untiring efforts in clearing our doubts are very much respected. You have patience, knowledge, logic and fairness in singularly great proportions. Hats off to you Arthur!

    True the behaviour of a cancer should vary from person to person understandably because irregular gene mutations are the root cause of the disease and thus the genomic differences. Hence the response to treatment cannot be predicted accurately or common rules cannot be established for all. Therefore controlling DHT by inhibitors may not have any positive impact on disease progression or survival benefit of some individuals and also some individuals may respond positively and they may benefit as you have correctly explained.

    But the moot point of David’s question is more serious than that. The difficulty in understanding the “upside down” position! The exactly opposite effect. According to whatever trials the possibility of 5-alpha reductase inhibitors “promoting prostate cancer” is not easy to gulp down.

    Best regards,



    Dear Sisara:

    Arthur says that the very small possibility that use of 5ARIs may promotes the induction of high-risk prostate cancer (when used to prevent prostate cancer in otherwise healthy men) has been around for years. This is not a new idea, and it is the reason that 5ARIs were never approved as a treatment to prevent prostate cancer here in the USA. We know that use of 5ARIs reduces risk for a diagnosis of prostate cancer in about 25% of such healthy men (but most of that reduction affects relatively low-risk forms of prostate cancer).

    Whether the perception that 5ARIs really can have the effect of promoting the induction of high-risk forms of prostate cancer is actually correct is a very highly controversial subject, and there is a large number of specialists in the prevention of prostate cancer who believe that this perception on the part of other physicians and regulators is completely misplaced and based on a mistaken interpretation of the available data.

    Arthur’s current view is that: there may be a very small possibility of such an effect; that is is not as yet proven that such an effect is “real”; and that individual patients need to make decisions about whether that risk is sufficient for them to outweigh the potential benefits in any particular circumstances. Arthur would observe that, as far as he is aware, there are no data whatsoever to suggest that the risk of diagnosis with prostate cancer is increased among the millions of men treated every year with 5ARIs for benign prostatic hyperplasia.

  146. Dear Arthur,

    Finally you have landed your jet plane in a very safe zone! – “benign prostate hyperplasia”. Beyond this territory only, the high-risk malignancy lies and it is cloudy and misty. The pilots beginning to say various things and the poor passengers are confused.

    You have said, 5ARIs were never approved in the USA for cancer treatment. Does this mean today Avodart is available in the US market and the cancer specialists are using same without the approval? Or later, the approval was granted? Both Proscar (finasteride ) and Avodart (dutasteride ) are available in our pharmacies too. Now I don’t want to use these much controversial 5ARIs.

    Arthur, thank you very much for adding a lot more new information in your last reply. When I argue with you, I learn more and more from you and increase my fund of knowledge. I hope I am not offending you or disturbing you in doing so.

    In all humility,



    Dear Sisira:

    Arthur would point out that no country, anywhere in the world, has ever approved the use of finasteride or dutasteride for the treatment of any form of cancer.

    These drugs are approved in some countries for the prevention of prostate cancer (but not in the USA). They are also used, off label, here in the USA by a significant minority of prostate cancer specialists for both the prevention of prostate cancer and for the treatment of progressive prostate cancer in selected patients. The latter use is almost invariably in combination with LHRH agonists and antiandrogens as part of a three-drug intermittent androgen deprivation therapy regimen.

  147. Dear Arthur,

    Thank you very much for taking lot of trouble to answer my questions on 5 ARIs ( originally raised by David ) from all angles. Now I am in full comprehension of all what you have said about approved treatment protocols and some isolated medical practices.

    Further, I manged to read a Drug Safety Communication message from the US Food and Drug Administration – “ARIs may increase the risk of a more serious form of prostate cancer”

    I think, this is a good take home message for my Gleason 9 disease, and is also in congruence with your explanation.

    Thank you once again.


  148. Regarding “Active surveillance common in Ontario; less so elsewhere in Canada”, are you not aware of what Dr Laurence Klotz is doing at Sunnybrook Hospital in Toronto, Ontario, Canada? I think his program is older and larger and documented in more published papers. I have been part of it for 10 years.

    John Leppik at


    Arthur responded:

    Dear John:

    Arthur says yes, both he and the Sitemaster are extremely well aware of what Dr. Klotz has been doing at Sunnybrook for the past 20 years. The Sitemaster has been reporting these data for years. What is interesting to both Arthur and the Sitemaster, however, is that despite all the Sunnybrook research and consequent data, the adoption of active surveillance in Canada but outside Ontario appears to still be relatively low.

  149. There are two different entry points for a prostate biopsy. One (less invasive and less painful, I am told) is entry via the perineum and the other is through the rectum wall.

    If the first is less invasive and less painful why do the second or TRUS?



    Arthur responded as follows:

    Dear Dick:

    Arthur is not so sure that the average urologist would agree that a transrectal biopsy would necessarily be any more invasive or painful than a transperineal biopsy. The vast majority of urologists do biopsies by the transrectal route, so when they are painful or thought to be invasive we are more likely to hear about it. In addition, there is the question of whether a standard, systematic, 12-core transperineal biopsy is as good at detecting cancer across the whole of the prostate as a standard, systematic, 12-core transrectal biopsy. The two different types of biopsy mean that the needles are entering the prostate from somewhat different directions.

    Also, you need to understand that TRUS guidance is used regardless of whether the biopsy is done transrectally or transperineally because the ultrasound imagery is essential to making sure that the biopsy needles are actually sampling tissue from the appropriately selected areas of the prostate.

    Arthur says that there is, in fact, a much better argument for the use of transperineal as opposed to transrectal biopsies, and that is that the transperineal route is associated with a lower risk for biopsy-acquired infections. Since, despite this well-understood risk factor, many of the best urologic oncologists in the world prefer to do biopsies by the transrectal route, it is probably the case that they believe this gives them a better way to conduct the biopsy and get more accurate results. Arthur does not know whether that is actually true or not. It would probably be extremely difficult to prove that categorically since it would require many, many patients to have two different types of systematic 12-core biopsy at the same time — and Arthur can’t see a lot of patients volunteering to be part of that study!

  150. Do we know of a cost comparison?


    Arthur responded as follows:

    Arthur says he hasn’t got a clue, but it is hard to believe that there’d be much difference, if any, for a standard 12-core systematic biopsy.

  151. Hi Arthur,

    I am new to this site. I sure hope you might have some insight for me. My husband has stage 4 prostate cancer and has been receiving treatment for the past 9 months.

    The last treatment he received was Provenge. That was 6 weeks ago and ever since the has has severe flu-like symptoms: pain, nausea and fatigue. The doctors say they have never seen this happen before. They keep telling us just to wait but he just seems to get worse. I cannot find anything on line related to this long term hyper-immune response. I even called the Dendreon company and they do not have information on it either.

    I am hoping that maybe you or one of your blog followers may have some insight.



    Arthur responded as follows:

    Dear Ellen:

    This is not going to be very helpful, but Arthur says he has been expecting there to be a very, very, very small number of men who were going to have this type of hyper-immune response to drugs like Provenge. He is sorry that it had to be your husband.

    Arthur says that any type of immunotherapy in an already immune-suppressed individual comes with a very small risk for very unusual immunologic reactions, because the therapy itself may trigger rare immunological effects that aren’t seen even in large clinical trials. Arthur is therefore not surprised that even Dendreon is telling you that they haven’t seen a hyper-immune response like this before. It’s not as though Provenge is being used to treat even hundreds of thousands of patients.

    What you and your husband should do about this is a whole different question. Arthur would suggest that you may want to see if there is a really good academic medical center near to you with a sophisticated immunobiology department or similar. Arthur’s concern would be that just as one doesn’t know one is allergic to peanuts until one first eats one and has an allergic response, neither your husband nor his doctors had any reason to know he was going have this type of hyper-immune response to Provenge until it happened. The question is going to be whether the response can be “turned off” again. Arthur doesn’t have an answer to that question — and he has never heard of an actual case like this before.

  152. Dear Arthur,

    I have written to you before but to summarize:

    I am 54 years old. I was diagnosed with prostate cancer when I was 49, 5 years ago, and 4.5 years ago underwent robotic surgery.

    Pre-operation: PSA: 5.8, with palpable DRE

    Pathology report: Organ confined, Gleason score: 3 + 4, one positive margin, 6% involved, no lymph node was examined.

    Since then in all my PSA tests have been undetectable (under 0.04) except once that it was 0.04 2 years ago.

    My latest PSA test came out as detectable at 0.06

    I was under care of a nurse practitioner and now she tells me I need to see the doctor in 3 months.

    I asked the nurse the following questions and will list her answers, will you please let me know of your valuable opinion on them:

    Q1: Is there any chance that the PSA goes back to undetectable or the genie is out of the bottle?

    A: Very slim chance

    Q2: Should I start a salvage therapy ASAP to not to loose the window of opportunity?

    A: No Doctor at this stage will start anything

    Q3: Isn’t having another test in 3 months too long? Shouldn’t this be done sooner?

    A: 3 months is the standard and no harm will come out of that.

    Q4: Is there any chance that this will never get to the point that further intervention is not necessary?

    A: Possible but not likely.

    Q5: What can i do meanwhile?

    A: Not much, follow up on tests and follow a heart healthy diet.

    I appreciate your valuable input,

    Best regards,



    Arthur responded as follows:

    Dear Abbas:

    Arthur has copied your questions and the nurse practitioner’s answers and then inserted his own comments in italic type below.

    Q1: Is there any chance that the PSA goes back to undetectable or the genie is out of the bottle?

    A: Very slim chance

    Arthur says that he thinks it is eminently possible that your next PSA result could come back again at < 0.04. However, it also may not, and the important issue in that case will be how fast your PSA is actually rising.

    Q2: Should I start a salvage therapy ASAP to not to loose the window of opportunity?

    A: No doctor at this stage will start anything.

    Arthur agrees with the nurse practitioner. No good doctor is going to do anything yet for the very simple reason that your PSA level might drop back down to < 0.04 again. And any form of treatment that can be given now could still be given with equal effectiveness in 3 months' time.

    Q3: Isn’t having another test in 3 months too long? Shouldn’t this be done sooner?

    A: 3 months is the standard and no harm will come out of that.

    Arthur again agrees with the nurse practitioner. You could plead with him/her to have your next PSA test in 2 months rather than 3 months by saying how anxious you are, but 3 months really would be completely normal — and reasonable.

    Q4: Is there any chance that this will never get to the point that further intervention is not necessary?

    A: Possible but not likely.

    Arthur thinks that if your PSA was to drop down again to < 0.04 in 3 months' time, then the answer is yes, there is a chance. But he agrees with the nurse practitioner that if the PSA rises again (say to 0.06 ng/ml in 3 months' time), then the answer is probably no.

    Q5: What can I do meanwhile?

    A: Not much, follow up on tests and follow a heart healthy diet.

    Arthur agrees entirely with the nurse practitioner about this. If you start to try to “do anything” at this stage, then we won’t get a clear idea of whether your PSA is really rising or not, and we will have no clue about how fast or slowly it is rising. We need that information to get a clear idea about whether it is really a good idea to do anything yet or not.

  153. Dear Arthur,

    This has reference to your above conversation with Abbas regarding a PSA issue.

    Is it correct to say a PSA level at 0.06ng/ml as “detectable”?

    I am under the impression a PSA level of 0.2ng/ml or lower should be considered as undetectable.(After having undergone a prostatectomy)

    Is there any other matter involved here?

    Your clarification would be greatly appreciated.




    Arthur responded as follows:

    Dear Sisira:

    Arthur says that the term “undetectable” is an historic term from when we started to use PSA testing in men who had surgery for their prostate cancer. At that time there were no ultrasensitive PSA tests, and so the best result you could get after treatment was a PSA level of < 0.1 ng/ml and people started to call that "undetectable".

    Arthur would also point out that, obviously, a PSA level of 0.04 or 0.06 mg/ml is actually "detectable" now that we have ultrasensitive PSA tests. There are actually research-type PSA tests today that can measure PSA level way, way lower than that, down to femtograms per milliliter as opposed to just milligrams per milliliter, but such tests have no clinical value.

    So … someone with a PSA level of 0.04 or 0.06 or even lower (e.g., down to about 0.003 ng/ml), measured with one of the ultrasensitive PSA tests that are available, does have a "detectable" PSA level. However, from a clinical point of view we really don't know if there is a meaningful difference between a man who has a stable PSA level of (say) 0.09 ng/ml and a man with a stable PSA level of 0.02 ng/ml. And we also know that ultrasensitive PSA results in an individual patient can vary a little, up and down, for all sorts of reasons. These tests are, as the term specifies, “ultasensitive”, so such variation should not be surprising.

    The important thing to be able to know, when using ultrasensitive PSA testing, is whether the patient’s PSA level is actually rising consistently or not over a period of time. A man with three successive PSA results over 9 months that go from 0.03 to 0.05 to 0.08 would clearly appear to have a rising PSA and this would suggest that he will need some form of follow-up treatment (but what and when would depend on individual circumstances). Conversely, a man with three successive PSA results over 9 months that go from 0.03 to 0.05 to 0.04 would potentially appear to have a stable PSA level of about 0.04 ng/ml, and most urologists would recommend just continuing to monitor the PSA of such a patient as opposed to rushing him into treatment.

    Arthur says it is not the actual PSA level alone that is important here. It is the variation in that PSA level over time that helps the doctor and the patient to define when additional therapy may be appropriate. Getting “hung up” on individual PSA levels at a point in time — especially when they are very low like this — is not a very productive exercise. Why? Because we really still don’t know whether we do any better to give salvage radiation therapy (for example) to a man who had surgery and whose PSA has gone from 0.03 to 0.11 ng/ml or whether we can wait to see if his PSA reaches 0.20 ng/ml (which is the standard definition of biochemical recurrence after surgery). On the other hand, it is almost certainly wise to give salvage radiation therapy to a man whose PSA rises from 0.005 to 0.010 to 0.015 ng/ml over the course of three successive PSA tests — because the chances are very high that his next test result will come back at 0.20 ng/ml and he has a PSA doubling time of about 6 months.

  154. Dear Arthur,

    Thanks a million for a very informative response again. One more question, considering that my previous PSA test 6 months ago was undetectable, is it safe to assume at best it was 0.03 and now at 0.06 I have a 6 months doubling time (at best) which is quite worrisome, or do we need three PSA tests to establish doubling time? Second question is that after my last test, I am trying a much healthier diet and have added mushroom powder and Pomi T as supplements. I am under the impression that this will not mask or alter PSA results, is this correct?

    Thank you once again,



    Arthur responded as follows:

    Dear Abbas:

    Making accurate judgements about PSA doubling times is very difficult when PSA levels are less than 0.1 ng/ml. Arthur certainly doesn’t think you can make a valid judgment on just two PSA levels. He would want to see at least three or four levels before anyone was coming to any conclusions (unless there was a very clear progression, e.g., from 0.03 to 0.07 to 0.11).

    With regard to whether any specific type of mushroom powder or Pom-T would “mask” rising PSA levels, Arthur doesn’t think we have enough data to know whether or not that is the case in men who have had first-line treatment for their prostate cancer. In Arthur’s view, it would probably have been better if you hadn’t started taking these products because we have no idea what impact they may be having on your PSA level, and there is no good reason to believe that they have any real clinical value at all.

  155. Dear Arthur,

    All what you have said is relevant and thank you very much for your quick response.

    Recently I completed reading the book A Guide to Surviving Prostate Cancer by Dr. Patrick Walsh, who is an internationally renowned urologist heading the Department of Urology at Johns Hopkins, and who is also an expert on prostate cancer. This book is almost like a “crystal ball” and it has the answer for any imaginable question on prostate cancer. (Still I reserve my right to ask from Arthur!).

    Dr. Walsh has emphatically advised not to go for “ultrasensitive” PSA testing, which can lead to various confusions. The standard PSA test is the most reliable and trouble-free blood marker to assess the status of the decease before or after treatment. The reading can start from 0.000 ng/ml and having three decimal places doesn’t mean it is an ultrasensitive test. For example my PSA readings taken using the standard test quarterly happened to be: 0.002, 0.001, 0.003, 0.008, 0.004. (It is important to do the test using the same lab and observe if there is any change in the testing methodology). My last test was done in April 2016.

    I will be concerned only if the quarterly readings show a clear indication of an increasing trend towards 0.1 ng/ml because passing 0.2 ng/ml is considered as a biochemical failure.

    In fact, when I first observed my PSA going up from 0.003 to 0.008, I was really upset and asked from Arthur immediately and I was fully calmed down with his explanation. Really there is nothing at all to worry about. There is a long way to go before thinking of PSA velocity, PSA doubling time, PSA density, etc. The more we learn the earlier we can get rid of this “PSA Panic”!

    Learning from Arthur is one sure way!

    Cheers to all and many thanks to Arthur.



    Arthur responded as follows:


    Just so you know … Not every expert specialist in the management of prostate cancer necessarily agrees with Dr. Walsh about everything, and Arthur know some highly respected clinicians who think using the ultrasensitive PSA test as a marker after treatment is really highly advisable … so long as the patient is advised to recognize that small variations in ultrasensitive PSA results are quite normal and need to be seen as such.

    Also, Dr. Walsh is no longer the Chairman of the Department of Urology at Johns Hopkins. He stepped down from that position several years ago now, although he does still work there. He also no longer does surgery.

  156. Dear Arthur,

    Thank you very much for updating me on the management of Johns Hopkins. I am in Sri Lanka, far away from USA and all I said was all what I learned from Dr,Walsh’s priceless book.

    I am really sorry if the information I provided happened to mislead any readers and thank you very much for the correction.

    Obviously, no one can continue in service for ever but I think Dr. Walsh’s unparalleled contribution to the field of urology has made him a legend which has in turn made him really immortal. I agree with you that there are cases where specialists’ opinions differ. In fact these are the instances very often I refer to you to get an unbiased view point. In doing so, I can also use my own judgement to argue with you if I don’t agree with your explanation and I have found this approach to be an excellent learning process.

    Your kindness is always appreciated.


  157. Dear Arthur,

    Whilst our last topic of discussion on the ultrasensitive PSA test” is still hot, I did some quick research reading and found an excellent article on the subject with some interesting facts.

    I quote at random a few catchy points here but request those who hesitate to accept Dr.Walsh’s advice on ultrasensitive PSA testing to read the complete article, which is brief but very enlightening. The web access is given at the bottom.

    — “PSA is not prostate specific despite being named as Prostate Specific Antigen.”

    — “When we go to ultrasensitive levels in PSA assays, many issues will crop up that will affect the accuracy on value, such as calibration problems with varying climatic conditions, clinical chemistry applications, etc.”

    From a study conducted in 2011 :

    — “This study carries an important caveat for the use of ultrasensitive PSA tests — hopefully men will become aware of this before making any precipitate decision based on what may not be as accurate a test as they believed.”

    A key learning point from the above study:

    — “Ultrasensitive PSA doubling time is often significantly more rapid than traditional (regular) PSA doubling time, potentially overestimating the risk of clinical recurrence.”

    However, freedom of choice is a fundamental human right and you may chose either PSA test according to your wish. In any case we have to obey the doctors who treat us and follow their advice too.

    Thank you Arthur for your time and guidance.


    Arthur responded as follows:

    Dear Sisira:

    Arthur would gently point out to you that the article your refer to, written by Arthur’s good friend Terry Herbert back in 2009, with one update in 2011, is a little out of date. It remains true that we have to be cautious about using PSA doubling times based on ultrasensitive PSA data. Arthur thought he had already made that point to you rather clearly.

    Indeed, the most recent “Revised and Updated” edition of Dr. Walsh’s book (Surviving Prostate Cancer) was actually published back in 2012 and so would have been based on data from about 2010 to 2011.

    Please feel free to use whatever test you like, but if you want to become knowledgeable on the ways to use any test in the management of prostate cancer, Arthur suggests you familiarize yourself with data that is rather more current and being published rather more recently. Alas, Terry Herbert will be unable to update that article himself since he passed away from his own prostate cancer a couple of years ago.

  158. Dear Arthur,

    Your exhortations are well taken with a deep sense of appreciation.

    In fact, I have been trying my best to keep myself abreast with the latest research in drugs, treatment protocols, radiation technologies, MRI scanning etc. related to prostate cancer management ever since I was diagnosed with prostate cancer. Some of these take decades to “move from the bench to the bedside” and and we may not see them at all in our hospitals here with very limited facilities. But it pays to be well informed, as I have realized that I should be the “manager of my own case”. I am not quite sure whether the doctors are interested in me!

    Being interested in the new approaches, I bought the book titled Prostate Cancer Breakthroughs 2014 by Dr. Jay S. Cohen very recently, and a couple of weeks after I finished reading the book I was saddened to learn that he had passed away in December 2015. He had been diagnosed with prostate cancer only in 2011. According to his book, though containing very useful information, he was over-confident on the new stuff and he avoided the gold standard curative treatments — surgery and radiation — being a strong proponent of “active surveillance”. (True there are many instances of over-diagnosis and over-treatment with these aggressive regimens which may cause severe side effects. But for a lethal disease of this nature, I think one should not take chances.)

    For your kind information, I have come to know about a new blood test called the 4KScore Test. This test was developed by OPKO Diagnostics in 2015. This test uses an algorithm that incorporates total PSA, free PSA, intact PSA, and human kallikrein-2 plus fa ew more variables to calculate very accurately the percentage risk of finding the presence of aggressive cancers of Gleason 7 and above. The test is said to have been studied on over 22,000 patients. This test can be very useful in diagnosing a prostate cancer accurately at a clinical level, and avoiding aggressive and more invasive procedures. Surely you may have more information on this test and I request you kindly to make same available for the benefit of the readers. (I cannot give a guarantee on the words of assay manufactures but you have the competence to pass your judgement.)

    By the way Arthur, I was glad to learn from you that the article I brought to your notice on “Ultrasensitive PSA” had been written by your good friend Terry Herbert. Frankly I didn’t know that it was his work. However, I had known him as the founder of the YANA website and I had known his cancer story entirely with his dedicated service and the brave fight unto his death in 2014. I have been an ardent member of the YANA Prostate Cancer Support Group since my surgery in March 2015.

    Thank you very much for finding a place for his article in our conversation here which can be read by others too for their benefit.

    After having written such a brilliant article based on solid scientific facts in 2009 and being able to update it in 2011, I think your good friend shall have no regrets about his inability to provide further updates due to his demise. Alas, neither Isaac Newton nor Michael Faraday lived up to the 21st century to update their great scientific discoveries!

    Best regards.



    Arthur responded as follows:


    Arthur says that if you enter the term 4KScore into the search system at the top of this page, you will find numerous references on a regular basis to the 4KScore test and its application in the articles by the sitemaster. This test was originally developed by the research team at Memorial Sloan-Kettering Cancer Center in New York and then licensed to OPKO.

  159. Wow! Dear Arthur,

    All these days I saw only your attractive picture with the cowboy hat but didn’t see the small search engine/box on top of this page – right side corner. It works well as you said.

    Thanks a lot.


  160. Hi Arthur, we talked before and now I have a query.

    Since treatment for stage III, Gleason 4 + 4 with seminal vesicle invasion, about 8 years ago, I have been OK, with a PSA of 0.1 and lately 0.01. I am 72 and also have had intractable paroxysmal atrial fibrillation for a long time.

    I have received no cancer treatment for the last 7 years. My treatment was a mix of EBRT and then HDR-BT, also Prostap 3 four times a year for 2 years. I am impotent. I am suffering a slow deterioration in my mental acuity, memory loss, etc. This is not being treated at all. I am reasonably active but hate walking but am quite active in the garden and round the house. I am taking a lot of supplements including Mortepa, CoQ10, B complex, K2, and liquid iron daily as my blood count tends to be low. However I lack energy and vitality and I can see my bone density and skin is deteriorating. I have some slight osteoporosis and damaged disks in lower back and severe damage in my cervical disks 5, 6, and 7. During my last medical, my new doctor commented on my testosterone being low, and this is the nub of the question:- In your experience, is it dangerous to take testosterone supplementation, when we know that prostate cancer is driven by testosterone?

    Many many thanks and best regards from Leitrim, R.O.I.



    Arthur responded as follows:

    Dear Mike:

    Arthur says that, over the years, there has been enormous controversy over the question whether testosterone supplementation is appropriate in men like you who are hypogonadal (i.e., have a low serum T level) after treatment for prostate cancer. However, …

    Arthur can tell you, too, that a lot more urologists, today, feel very comfortable giving testosterone supplementation to men like you who have shown no sign of any recurrence of their cancer after a significant period of time than they would have done 5 or 10 years ago. What Arthur also has to tell you, however, is that there is going to be some degree of risk for prostate cancer recurrence, but in your case it may be very low. If you can, Arthur suggests that you need to have a very specific discussion about that risk with your doctors and then come to a shared decision about whether this is something you are willing to try. There is no “right” or “wrong” answer here that Arthur is aware of. It is all a matter of the potential balance between benefit in terms of possible improvements to you quality of life and risk in terms of a cancer recurrence.

    If you do decide that you want to try this, you also want to talk to your doctor about frequent (e.g., every 3 months) monitoring of your PSA level for at least the first year after you start the testosterone supplementation so that you can be very sure that you catch any sign of a recurrence as early as possible and can stop the supplementation again promptly if that seems to be necessary.

  161. Dear Arthur,

    Thanks very much for your prompt and well considered response. I have arranged to see my radiologist in June in the Mater Private Hospital in Dublin. I was in contact with him today via his secretary, and explained the situation but she reverted to me within a few minutes, saying he was emphatically of the opinion it would be wrong for me as “my margins were too narrow”. So I will hold fire until I see him when I hope to have a full and frank discussion with him on the matter. I think he is of the old school and is unlikely to have a change of heart! I will let you know what happens.

    Best for now,


  162. Dear Arthur,

    This is further to my previous conversations with you regarding various issues relating to prostate cancer.

    I am just trying to understand more clearly what is happening to my cancer with the ADT continuing for 2 years after RP and IMRT. I just started my second year on ADT in April. My pathological staging was T2cN0M0, Gleason 4 + 5 = 9. I understand clearly that the treatment has to continue although my PSA up to date remains at 0.00 ng/ml since RP because there can be residual cancer cells that escaped from the prostate gland even before surgery due to the highly aggressive nature of my cancer.

    Please explain to me the following points which may sometimes sound theoretical but it will help me to get my doubts cleared.

    1. If my residual cancer cell volume was 100,000 cells at the time of starting hormone therapy, after completion of 1 year with zero PSA,
    Is the volume remaining same or could be decreased or could have increased even without affecting the PSA value?

    2. Is it correct to assume at an undetectable PSA level, these 100,000 cells are not proliferating and therefore the cancer progression has been arrested?

    3. In this 100,000 cell volume always there is a certain percentage of cancer cells which are hormone-insensitive and what can the hormone treatment do to them? Won’t they progress silently without even producing any PSA and deceiving us during the ADT period?

    4. Suddenly, if the PSA goes up to 5.00 ng/ml that would definitely indicate a cell volume increase (proliferation/cancer progression) say for example up to 500,000. With a different treatment protocol (hormone type), if the PSA is brought down to undetectable level again, what does that mean? Any reduction in cancer cell volume? Or we are playing only with PSA numbers without any significant impact on disease control?

    5. After RP and IMRT both being “gold standard” curative treatments, if the presence of any further residual cancer cells is suspected, why go for palliative treatments such as ADT, allowing hormone-insensitive cells to take the upper hand and, at some stage killing the man, without using cytotoxic treatment strategies to kill the remaining cancer cells before that could happen?

    Good day!



    Dear Sisira:

    Arthur says your questions are entirely unanswerable because human biology is not a form of engineering.

    No one else has ever had your prostate cancer in your body. All that doctors can ever do with someone with an aggressive form of cancer like yours is “the best they can”. It is certainly true that you could, and it is arguable that you should have chemotherapy as well as the androgen deprivation therapy (ADT). Whether that is the “right” thing to do for you specifically is unknowable; you’d need to discuss that with your doctors. If you were going to do that it should probably have been done several months ago if you wanted to give it the best shot. But then chemotherapy also comes with a whole spectrum to side effects.

    As Arthur knows he has told you before, how individual men will respond to ADT (alone or in combination with radiation therapy) is utterly unpredictable. In some men there are indeed ADT-resistant cells at the time of initiation of therapy and that cell clone grows rapidly after initiation of treatment. In other men it appears that ADT-resistant cells may take decades to develop and take hold — and then there is the entire spectrum of possibilities in between.

    With regard to the use of ADT for 2 to 3 years in combination with radiation therapy, Arthur would note that this is not simply the addition of palliative care to the radiation. Such combination therapy has clearly been shown to increase the probability of long-term survival among patients so treated by comparison with radiation therapy alone and by comparison with ADT alone.

    Arthur says you are trying to apply the principles of chemistry and physics to disease in an individual patient. But biology doesn’t work that way; different individuals can respond very differently to even simple, standard forms of therapy. And you also need to appreciate that a “gold standard” form of treatment doesn’t mean that something is necessarily “curative”. Such treatments are commonly given “with curative intent” but their ability to actually cure the cancer in an individual patient is utterly unknowable in advance (or even for years afterwards).

    And if your PSA was to suddenly start rising tomorrow, exactly what would need to be done (or even could be done) about it depends — first and foremost — on exactly where the recurrence is occurring, why it is occurring (which may or may not be knowable), and what potential treatment options are available. It’s not as simple as what the effects of some other particular form of drug treatment might or might not be on your PSA level.

  163. Thank you very much Arthur,

    What you have said is the stark truth about the prostate cancer. Particularly, my specific prostate cancer created by my own gene mutations and DNA specifics that it is merely impossible to predict by comparing with any known model. Just like my ‘thumb print’ which does not match with anybody else’s.

    There is hardly anything I can disregard in your honest explanation and I agree that there are limitations in understanding human biology. It is more correct to say these limitations apply only to ourselves and not to the scientists. Only for today and not for tomorrow!

    When I read about the findings of genetic engineering, I hesitate to uphold your view that human biology is not a form of “engineering”, rather it could be re-engineered using advanced scientific measures. It is happening in this decade and revolutionizing the fields of surgery, radiation, drugs and treatment strategies for cancer.

    Please take my question (cancer) out of my body to a vacuum and give one more try to provide a “theoretical’\” answer if you feel it worth your while.

    Question: At a PSA level of 5.0 ng/ml my cancer volume was 100,000 cells. I took hormone treatment (ADT) for 3 months and now the PSA level is 0.00 ng/ml (undetectable). What are the possibilities?

    (a) 100,000 cells remains same without proliferation because they don’t have food (hormone) for their growth. For no cell activity, no production of PSA.

    (b) Cell volume might have increased along with time because still there are androgens in the body, especially DHT to support proliferation. But the action of ADT keeps the PSA at an undetectable level for some time.

    (c) There is also the possibility of some cancer cells to die making the original cell volume lesser than before.




    Dear Sisira:

    Arthur says that you should not make the mistake of thinking that just because we now have the ability to manipulate very small and very complex molecules (genetic and biochemical “engineering”) that the principles of normal engineering can be applied to the management of human disease. These are two very different issues. We know enough about normal engineering (the building of skyscrapers, for example) to be able to create functioning structures that can exist for thousands of years, (e.g., the pyramids in Egypt). By comparison, we know almost nothing about how to change a human body in a lasting way without having other effects that will be seriously damaging (side effects). Interestingly, of course, when we practice normal engineering on a large enough scale (as we now have and do), it also has serious side effects (global warming) on the entire planet.

    With regard to your question, Arthur says you are forgetting that in your body new cells are formed and old cells die routinely, on a daily basis. In most men with prostate cancer, ADT will hasten the death of most prostate cancer cells by cutting of the needed supply of dihydrotestosterone (DHT), but all prostate cancer cells are not the same. What matters is not the total number of cancer cells. What matters is whether cancer cells continue to exist in the patient that have the potential to metastasize. Since we don’t understand what makes a cancer cell metastasize, Arthur can’t tell you exactly why some men who have radiation + ADT will have long-term stable disease and why others will have progressive disease relatively soon. No one can tell you that. It may have something to do with the theory behind what are known as “cancer stem cells”, but that theory is unproven at present despite intense research work in this field.

  164. Dear Arthur,

    To my knowledge there is nothing called “normal engineering”. To be specific “civil engineering”, mechanical engineering”,”electronic engineering”, …, and many many so to speak of. But in disease management and analysis, genetic science and molecular science have come to the fore in engineering the aspects of microbiology to develop advanced drugs to treat cancer. That is simply the context and building construction type of engineering has no relevance at all in our topic.

    Truly there are some learning points in the second part of your answer. But my question is not “What is going to happen to me?”, the question you have many times reminded me that nobody could ever answer. You are correct. Such questions should be asked only from astrologers and there are plenty of them in my country. Some people believe they can cure cancer too in addition to their predictions! The answer I am seeking is totally different. It could be answered only with some knowledge in “cancer biology”, by taking into consideration the cancer cell volume, cancer cell activities, and the blood marker PSA as the indicator. It would be better to treat the question as hypothetical. The focal point of my question is ‘whether a drop in PSA to zero indicates a reduction in cancer cell volume from its original size where the PSA was 5.0 ng/ml or the treatment causes only a stoppage to the synthesis of PSA by ADT whilst the cancer volume (cell population) is silently progressing. I think this is what you have explained correctly when you said in some men progression may take years and in some it may happen soon after having been treated with ADT + radiation.

    I also agree that this situation becomes more complex since prostate cancer is not homogeneous and does not follow the usual programmed cell mitosis and apoptosis like normal cells due to DNA damage.

    In effect what I would now like to infer is the PSA test in this situation is deceiving us to some extent about the silent progression of the cancer. It will ring the alarm bell only when the cancer cells become hormone refractory and begin to metastasize whilst we remain complacent, missing the early opportunities of doing something to kill the cancer or putting stronger road blocks to stop its lethal progression.

    This may be why doctors don’t want to answer our questions. They only expect us to sit and look around! Wait until the turn comes!

    Thank you indeed Arthur for being different. For not being a Doctor and taking so much trouble to help us with your singular generosity.


  165. The link to “Prosdex” on page appears to be broken.


    Arthur responded as follows:

    Dear Chris:

    Arthur says that, according to the Sitemaster, that link is not actually broken. Rather, the original site has been shut down.

  166. Dear Sisira:

    Arthur trained many years ago as a biochemist with a subspecialty in molecular biology. He has so many disagreements with your perspective that this conversation has become meaningless.

    Your mindset is betrayed by your proposed inference that “the PSA test in this situation is deceiving us to some extent about the silent progression of the cancer.” The PSA test measures one thing and one thing only: the amount of PSA in your blood stream at a point in time. This may or may not, under specific circumstances, have anything to do with the number of cancer cells in the body of an individual patient. It is reasonable to assume that it should do so, under most circumstances. It is not reasonable to assume that that must be the case, however.

    Arthur says that there are good physicians and there are bad physicians. There are also physicians who are good communicators and those who are bad communicators. And then there are questions like yours that are of very little interest to most physicians because they can’t answer them. If you want an answer to your question, you are correct, you would have to conduct a complex biological experiment (of no therapeutic value) in about 200 or so men, and then you could find out what the ranges of the ratios of PSA level to cancer cell count might be in the specific tissues sampled over time … but it still would have no therapeutic meaning because it wouldn’t be predictive and it would only be meaningful in relation to the specific tissue sampled. Arthur would point out that PSA test is not, repeat NOT, a test for risk for prostate cancer progression. It is you who are making a mistake if you are “misled” into believing that the PSA test is an indicator of risk for progression. It isn’t. It is only a test that can tell you (or your physician) when a cancer has started to progress in a very specific way (by cells leaking more PSA into the bloodstream).

  167. Dear Arthur,

    If “crystal” is the most appropriate and ultimate adjective, your answer is crystal clear and flawless! I am no more in a mist.

    On the contrary, it is not easy to challenge a person like you and get the best of best.

    I owe you a great deal of thanks.

    You are much admired and appreciated.


  168. I am not sure if this is the place where a question to “Arthur ” is posted.

    I had EBRT for Gleason 9, T3 disease in 2010 with hormone therapy since 2010, and now my PSA is rising, now about 2.0.
    Following MPsa PET scan with gallium-68, the doctor at Epworth Hospital in Melbourne has offered IMRT and Calypso for PG. Is this wise? What are the side effects?

    The doctor said the scans show very tiny mets to 2 lymph nodes, but cannot give details, and no indication of incontinence; I suspect some info is withheld. Should I proceed with IMRT?

    Regards, Patrick Turner, in ACT.


    Arthur responded as follows:

    Dear Patrick:

    Yes, that was the right place. However, …

    Arthur says that he is missing a lot of information, and so the guidance he can offer you is very limited, but here it is for what it is worth:

    (1) Arthur says that if you think that “information was withheld” from you, then you should call the doctor’s office and politely state that you are worried about what you might not have been told and ask to speak (politely) to the doctor again. However, you do need to understand that there are going to be questions that the doctor just can’t answer because he doesn’t know the answers.

    (2) If you have a rising PSA after 6 years on androgen deprivation therapy, then you now have castration-resistant prostate cancer. Stopping the progression of such a cancer is going to require aggressive treatment of some form, and all such treatments come with risks for side effects — but most of them can be lived with.

    (3) Arthur cannot tell what you mean by radiation of the “PG”. This is not an abbreviation he has ever seen before so it may be an “Australian-ism”. Arthur assumes (always dangerous) that you are referring to Calypso-directed IMRT to some predefined region of the pelvis, with an especial focus on the area with positive lymph nodes. (You may simply be referring to the “pelvic girdle”.) This is now a relatively common form of procedure, and the risk for side effects is actually rather low by comparison with what it used to be (because of targeting technology like the Calypso system). You really need to ask the radiation oncologist exactly what the most common side effects are that he or she sees associated with such a technique in his or her practice, but Arthur wouldn’t expect any really serious side effects from such a treatment today in the vast majority of cases.

    (4) You say that the doctor “cannot give details, and no indication of incontinence”. Arthur doesn’t know what details you are looking for so he can’t help you with that. As for incontinence, Arthur knows of no good reason to believe that such treatment would lead to any serious form of incontinence today, although radiation therapy of the lower abdomen always comes with some risk for temporary diarrhea. A lot would depend on the dose of radiation being given (which would probably be relatively low to an area like this) and the precise area that the doctor expects to radiate.

    (5) Arthur cannot tell you whether you should or shouldn’t have such radiation. That’s a decision only you can come to in discussion with the doctors. What he can tell you, however, is that if he was in your situation, and all his assumptions about exactly what is going on were accurate, then Arthur would certianly be willing to try the radiation himself, and he would also be asking the doctor whether there was any potential value to combining the radiation with a course of treatment with a drug like abiraterone acetate (Zytiga) or enzalutamide (Xtandi) to see if the combination of the radiation and the drug therapy could stop the growth of the castration-resistant prostate cancer cells.

    Arthur hopes this is helpful.

  169. Hi Arthur. I live in Southern California and all indications are I will be diagnosed with prostate cancer after an MRI-guided biopsy soon. If I would require and choose surgery, I would like it be done at the best hospital for this in Southern California, and the best and most experienced surgeon that has done hundreds in his life time, and at least 60 per year (per Dr. Patrick Walsh, an authority in this area). Which hospitals/doctors in Southern California are the best of the best? How do I determine that? I am now with Kaiser, but I am prepared to go outside Kaiser and pay out of pocket (if I need to). I know the cost differs from hospital to hospital, what do you think is the range of costs for open prostate surgery? Robot-assisted? What is the best way to get cost information since most hospitals are not transparent when it comes to cost? Appreciate your help.


    Arthur responded as follows:

    Dear Solomon:

    Arthur is not and could not possibly pretend to be any sort of expert on “who is the best” surgeon, radiation oncologist, etc., in any specific area of the country. Determining that would be a full-time job in and of itself (always assuming one could find the data to do it accurately, which is doubtful).

    Arthur says your best bet is to contact the support group leaders for Us TOO chapters in the major areas of southern California and ask them their opinions. You can find contact information for such individuals if you click here.

    With respect to obtaining pricing information for surgery if your insurer won’t cover specific institutions, all that Arthur can really tell you is that you need to be a really tough negotiator because the hospitals are probably paying your insurance company half or less of the “rack rate” that you will be told. If you look at this web site, you will be able to see what the “real” costs are for prostate cancer surgery from an organization that is seeking to bring some transparency to this issue for people like you.

  170. Hi Arthur,

    Thanks for the response.

    I am seeing my oncologist today, who probably will give me Casodex and put me on monthly injects of Lucrin for ADT. PSA now 2.3, up from 1.5 a month ago. I see a urology surgeon next week to discuss possible bladder and PG removal and stoma for external urine bag. A friend here is happy and cancer-free because of the far more radical surgery. In 2 weeks I will see the radiologist who did the original EBRT in 2010 to discuss side effects of proposed Calypso IMRT, which probably is a good idea between now and future surgery or start of chemotherapy. You are right, combined chemo can work well, I saw some research on survival time.

    I’ve calmed down a bit after learning there’s a tiny spread to two lymph nodes; the doctors are not sure where yet. It takes time to get to see the specialists because they have maybe another 100 patients, and some are in greater need than I am. The latest 3D PET scans with gallium-68 are a marvel, but my GP could not see the scan properly on his computer, and I don’t know if the oncologist can either — they are sometimes behind with latest technology! So the delays are painful because you know the cancer isn’t waiting around.

    We all have to die, that’s the bottom line, and cancer treatment often doesn’t offer a cure, but it offers us all time, and freedom from pain if we are lucky at the end.

    I was Gleason 9, T3, PSA 5, age 62, and doctors opened me, then decided not to continue with RP; too much cancer present, hence the HT and RT. I got more promises about a fix, but the doctors didn’t know any more than I did about just how bad my type of prostate cancer is, and it seems I am radio-resistant, and now becoming castration resistant too; cancer mutates slowly to outwit all attempts to stop it, it even makes its own testosterone to be able to keep going. The Calypso IMRT might work, but might not. The doctor who does the repeat RT claims all 45 patients he treated had a progression-free result later, i.e., cancer stopped, but it sounds too good to be true.

    I have a website page to show fellows what might happen to them. I am otherwise well, and I’ll be riding a bicycle 17 km to the hospital to see the oncologist. He likes to see me looking so well, dressed in Lycra, and with BMI 25, and not on 10 other medications for three other problems.

    We can only achieve the possible. This may seem impossible when we try, but try we must.

    Best regards,

    Patrick Turner.

  171. Hi,

    Of all the men who go through PSA screening for 15+ years, what percent are eventually diagnosed with prostate cancer (all grades)? In other words, what is the likelihood a man would get a prostate cancer diagnosis if he is screened with PSA for 15+ years?


    Arthur responded as follows:

    Dear Mark:

    Arthur says he talked with the sitemaster last night and neither Arthur nor the sitemaster know the answer to your question for the simple reason that, as far as we are aware, no one has ever followed a group of “normal” men who had PSA tests every year for 15 years.

    Arthur would point out that the answer to your question would, in any case, be highly age-dependent. In other words, if you started screening men for 15 years when they were 45, then a smaller percentage would get diagnosed during the next 15 years than if you started screening the same group of men when they were 55.

    Arthur would also note that you would be likely to get a different answer depending on the risk levels of the men involved because some sets of men (e.g., African Americans, men exposed to Agent Orange in Vietnam, men with a genetic or family history of prostate cancer) are at higher risk than that of the average Caucasian male.

  172. Arthur:

    I am 76 years old and was diagnosed with Stage 1, Gleason score 6 prostate cancer about 11 months ago. My PSA was somewhere in the 6-7 range. My DRE was normal at that time. I had both a prostate biopsy and, following the diagnosis of cancer, a whole body MRI which was clear.

    My urologist and I decided to initiate active surveillance and, since then, I have had two additional PSA tests, the first of which went down to 5.82 and the next went up to 7.42. At that point my doctor scheduled another biopsy, conducted last month, and I met with him today. The Gleason score has increased from 6 to 7, consisting of 4 + 3, which I understand is better than 3 + 4.

    We discussed treatment options and, although he recommended continuing active surveillance, he said if I decided to initiate treatment he would recommend either regular radiation treatments or cryotherapy. He didn’t recommend brachytherapy — seeds — Im’ not sure why.

    I am now trying to decide on:

    (1) Whether to initiate treatment or continue on active surveillance
    (2) What type of treatment to have … My tendency is toward cryotherapy if I have any.
    (3) Get a second opinion from some place like Johns Hopkins or Emory Cancer Center … I live in the Atlanta area … or somewhere else I haven’t found yet.

    I am scheduled to see him in 4 months and have another PSA test and, depending on the results, think about another biopsy.

    I plan on sending him a letter and advising him that I am seeking a second opinion before I decide how to proceed. Do you have any recommendations on how I should proceed. Do you have any second opinion providers other than the ones I listed that I should consider? Thanks for your help.


    Arthur responded as follows:

    Dear Jerry:

    Arthur says the first thing you need to do is check with your urologist about your revised Gleason score. A Gleason score of 4 + 3 = 7 is actually riskier than a Gleason score of 3 + 4 = 7, so either you misheard your doctor and your Gleason score is really 3 + 4 = 7 or you misunderstood him and he actually told you (correctly) that a Gleason score of 4 + 3 = 7 is less good than a Gleason score of 3 + 4. It is very important that you clarify this.

    Arthur says that the second thing that you might want to do is use the male prostate cancer life expectancy survey on the Memorial Sloan-Kettering Cancer Center web site to see what your risk is of actually dying of prostate cancer if you have no treatment unless and until it was absolutely necessary. What this survey will tell you is what is likely to happen to 100 men like you over the next 10 to 15 years if they get no first-line treatment (like radiation therapy or cryotherapy) for a prostate cancer like yours. Arthur cannot complete this survey accurately for you because he doesn’t know all of your health history. What he can tell you (based on the data you have provided) is that even if you are a very healthy 76-year-old who has never smoked in his life and if your Gleason score really is 4 + 3 = 7, then you would only have a 9% chance of dying of prostate cancer in the next 15 years, whereas you would have a 69 percent chance of dying of something else in the same time frame.

    Now, the question of whether to get a second opinion and where to get it is a good one, and there are certainly excellent physicians at Emory and at Johns Hopkins who would be able to give you such a second opinion. Getting an appointment to see him might be difficult but Dr. Martin Sanda, the chairman of the urology department at Emory, is a highly respected prostate cancer specialist, for example. And he originally trained at Johns Hopkins too. If your current urologist is a good one (and he certainly seems to be from what you have told Arthur above), he is not likely to have a problem with you seeking such a second opinion.

    The question of what type of treatment to have if you decide you need treatment is a much harder question because men of your age are at higher risk for the side effects of treatment than men in their 60s. As we get older we are all likely to find that we can’t recover as well after invasive forms of treatment (including radiation therapy and cryotherapy) than when we were younger, and so the critical issue for someone like you is not just what type of treatment to have if you want to have treatment but also the skill and experience of the person who is going to carry out the particular type of treatment you select.

  173. Hi Arthur,

    I’m new to this site but at 57 years old had a da Vinci radical prostatectomy in March just gone. I had my first results yesterday and was disappointed to hear that I had a PSA reading of 0.025. My doctor told me that he wasn’t sure if my levels are still dropping or if something has been left behind that may require radiation. He is making another appointment for 3 weeks time to do another test before making a decision. What sort of result should I be looking for and is it all a bit too soon. Also, when I had my blood taken, the nurse said she wasn’t sure which specimen bottle to use for a sensitive test and just used a normal one. As I said, I am new to this but am concerned after yesterday — I obviously hoped everything would be fine!

    Any advice at this stage??

    Many thanks.

    Nick — UK


    Arthur responded as follows:

    Dear Nick:

    Arthur says that if your surgery was in early March then there has probably been at least 12 weeks since the operation, which is certainly long enough after the operation to get a first PSA test. On the other hand, if your surgery was at the end of March, then it may only have been 10 or 11 weeks since the surgery (which is a very small difference) but there are surgeons who think that one should always wait 12 weeks. And there are no “rules” about this.

    Arthur notes that the other thing you need to understand is that your PSA level of 0.025 is actually well within the “undetectable” range since it is significantly less than 0.1 ng/ml. No one’s PSA level ever goes to absolute zero, and your’s might still drop down to (say) 0.005 ng/ml or thereabouts so Arthur doesn’t think there is any reason to start panicking. You just need to get a repeat PSA test as recommended, and hopefully the nurse will have made quite sure which vials she is meant to be using for the ultrasensitive PSA test by then too! Arthur certainly wouldn’t let anyone radiate his if he was in your situation and his PSA was stable at 0.025 ng/ml.

    Of course if your PSA starts to rise a little again, then that’s the time you and the doctors may need to start talking about the possible need for radiation therapy.

    Arthur would point out that the other thing that is relevant to all of this is what the full results of your surgery were. In other words, if you had a Gleason score of 8 to 10 and a positive surgical margin after the surgery, then you are in a very different situation to a man who had a Gleason score of 6 with very clear indications that all the cancer was confined to the prostate.

  174. I have checked back and my biopsy gave results of PSA 6, Gleason 3 + 3 disease (15%). MRI suggested T2N0M0. Not sure what all of that means. All the indications after surgery were that it had been confined and that there had been no spread. Does that make it better or worse?

    Thanks again for any advice.



    Arthur responded as follows:

    Dear Nick:

    Arthur says to forget about what happened before surgery (except for your pre-treatment PSA level). You now have accurate information about what was found at and after surgery.

    If your Gleason score after surgery was still 3 + 3 = 6, you had T2N0M0 disease, the cancer was completely confined to the prostate (no positive surgical margins, no positive seminal vesicles, no extracapsular disease, no positive lymph nodes), then there is every good reason to believe, with a PSA level of 0.025, that your cancer has been eliminated.

    Arthur says you do need to keep monitoring your PSA every 3 months or so for some time, just to make sure that there is no sign of a recurrence, but if the above is the case, then you have every good reason to believe you have had the cancer eliminated. Arthur also thinks you shouldn’t even be considering any radiation therapy unless there is a very clear sign that your PSA starts to rise again. Remember, no one’s PSA goes to absolute zero after treatment.

  175. Dear Arthur,

    I have been reading your response to Nick. Mine is T3N0M0 with Gleason 8 histology; was T3b in old speak. I think the 3 is due to invasion of the seminal vesicles. I had HDBT and 2 years on Prostap 3. My PSA is now at 0.01, and has been around that for last 6 years at least. I am in my 73rd year. Recently my T score was 5.5, but when I asked the oncologist could I use supplementation he said, “my margins were too narrow”. Is there any organic treatment that would be beneficial and help to delay the consequences of low testosterone?

    Thanks as always Arthur and colleagues,



    Dear Mike:

    Arthur says that (a) a diagnosis of clinical stage T3b disease is still “current speak” and does indeed mean that you were thought to have cancer that had spread into your seminal vesicles and (b) that most doctors are still unwilling to consider giving testosterone supplements to men like you because they worry that this will stimulate disease recurrence. However, …

    Arthur would also point out that attitudes are changing about the use to testosterone supplementation for men like you, and you might want to consider getting a second opinion from another specialist.

    You may want to have a look at this article and this article on our news web site that deal specifically with this issue.

    Arthur says that the bottom line is that testosterone supplementation in men like you is risky — but some men are willing to take that risk and some doctors are more willing to take that risk with their patients than others. (Most physicians, by their very nature, tend to avoid taking this sort of risk.)

    With regard to whether there are dietary and other methods to raise testosterone levels in men like you, there are a lot of products that claim to do this, but very little actual evidence of actual effectiveness. But Arthur claims little to no expertise on this issue because he is a great believer in just eating well and exercising regularly as opposed to using supplements of any type.

  176. Are you aware of anyone that has succeeded in getting Medicare to pay for a focal laser ablation for prostate cancer? Is there a web forum where I can ask this question and reach many people?


    Arthur responded as follows:

    Dear David:

    Arthur thinks your question is a very reasonable one. Alas he doesn’t have a good answer for you because (as far as he is aware) almost no one to date has tried to seek Medicare reimbursement for FLA because most of the patients who have had FLA have not been Medicare patients.

    There are two good places where you could try asking this question that Arthur is aware of. One is the Prostate Problems Mailing List. The other is the prostate cancer-specific Healing Well forum. However, Arthur is less than certain that you will be able to find anyone with the experience you seek on those forums either.

    The other thing that you could try is contacting the Medicare State Health Insurance Assistance Program (SHIP). SHIP is located in all 50 states so you’d need to find the right person to talk to in your state, but Arthur’s understanding is that SHIP can sometimes be helpful with all sorts of odd issues like this.

  177. Hi Arthur.

    Help for a worried newcomer to possible PCa

    A little about myself. Live in the UK and am 58 years of age no other health problemss (as far as I know).

    10 years ago when I was 48 went to the doctor’s because of frequent urination, needing to find a toilet when I was out more often than usual, etc. Doc did a DRE which she thought was normal and had the blood taken by the nurse. … May have been blood first then DRE; cannot remember. Phoned for results and told results fine nothing to worry about. (I have now found out that the PSA was 1.2.) Fast forward 8 years to 2014 when I go to the doctor’s again with similar problem as I was getting up maybe twice a night to go to the toilet. This time DRE (nothing unusual found) and a blood test the following day. Doctor called me in a couple of days later and said that my PSA was 3.3 and, because here in Britain the cut-off for my age group was 3, she recommended a trip to the hospital.

    I freaked a bit and said could I think a bit as I was only just over the line? … Went home and did some research and found that DRE first before the blood, etc., etc., plus I had ridden my bike the day before. Went back to doctor to explain. She agreed to another PSA; this time 3.1. She saw my reticence about going to the hospital (maybe big mistake) and agreed that it was possible that I had a higher than usual baseline, so we would do a PSA test every 6 months.

    Two subsequent tests both stayed at 3.1 and I think (know) I got a bit complacent and waited 14 months before going back, and then because I was having a bit of lower back pain. Then last week, 1 day before the arranged PSA test, I woke up very early with a very painful lower abdomen pain which proceeded through the day to refer itself to the testicles. (Felt as though I’d just been kicked in the balls.) This lasted all day but was better the following day. Following day had the blood test (no DRE) and walked out whistling. Got home Friday evening to an Answerphone message to ring the doctor’s surgery.

    It was at this point that I started to get a bit panicky as the onus is nearly always on the patient to phone the surgery not vice versa, plus the test was only the previous day, so I had visions of alarm bells and klaxons going off at the lab. (Never a good idea to be a pessimist.) So I spent a terrible weekend (doctor’s office closed all weekend) doing plenty of Internet research (probably not a good idea…), and fighting all kinds of imaginary monsters. Rang Monday and got a late afternoon appointment; was pretty much expecting the worst when I walked in.

    Doctor said that my PSA had gone up to 7.5 (I was a tad relieved as I was imagining double or even treble figures). He did a DRE and said that the prostate felt slightly enlarged but felt “normal”; arranged a urine test and some more blood for kidney function etc. I walked out of there feeling a great weight had been lifted as I know that a UTI which I have the symptoms of (groin, lower abdomen, and lower back pain) was also in the doctor’s mind.

    Fast forward a couple of days; results in; I don’t have a UTI, so I now have to hope for prostatitis, … or the rise in PSA I guess will be due to prostate cancer. I have now noticed some tingling in my left leg and foot; that along with the hip, back, and groin pain, plus a small amount of blood in the urine. Am I now looking at advanced prostate cancer? I know it could be prostatitis but I’m really worrying now. … Have been referred to the urology clinic (within the next 2 weeks).

    I know I’m jumping the gun and I do apologise up front for being a bit of a neurotic “cry-baby” (especially when I read about what some people on the different forums have gone through) but I just would like some advice. … Do you think that a PSA reading of 7.5 could be advanced stage/metastasized? I know you don’t have a crystal ball but from what I read you do seem to possess a lot of hard-won knowledge.

    Many thanks in advance and sorry for the long winded post.



    Arthur responded as follows:

    Dear Tony:

    Arthur says there are numerous reasons why a man of 58 years of age might have a PSA level of 7.5 ng/ml, up from about 3 ng/ml a couple of years earlier. These include include benign enlargement of the prostate (hyperplasia); an actual prostate infection or UTI; a form of prostatitis known as chronic pelvic pain syndrome (CPPS) and type III prostatitis (which is an inflammatory condition as opposed to an active infection); calcifications in the prostate (like kidney stones in the kidneys); and prostate cancer.

    Arthur also says that the chances that a man of 58 has metastatic prostate cancer with a PSA level of 7.5 ng/ml are very, very low indeed. Can this occur? Yes it can. Is it likely in your case? No it isn’t — but, as you point out, Arthur doesn’t have a crystal ball and it is possible.

    Arthur would point out that you are guilty of not taking your health care seriously enough! (A common male behavior!) So … you are gonna need to “man up”, go to the urology clinic, carefully and patiently explain for the urologist the history you have told to Arthur, and then listen with care! If you take the full written history that you wrote out above for Arthur, this may help you not to forget anything.

    It is likely that a good urologist will want to give you a cystoscopic examination and a prostate biopsy. Bite your lip and say, “Yes doctor!”

    It is quite impossible for Arthur to tell you what your particular problem is. You might have prostate cancer and you might not. What you do quite certainly have is a clinical problem that needs to be accurately diagnosed and then managed appropriately.

  178. I have been on Zoladex for 2 years. My surgeon and I have decided to continue with this to avoid a flare.

    My PSA is undetectable and near 0 for over a year now.

    Does prostate cancer bone metastases produce a higher PSA? Is a PSA test going to show a higher level just from bone lesions?

    Thank you


    William Donelson


    Arthur responded as follows:

    Dear William:

    Arthur says it is not at all clear to him why you are on the Zoladex.

    So long as you are on a drug like Zoladex and it is working well and you don’t become androgen resistant, then your PSA level should remain at < 0.1 ng/ml. However, conversely, the longer you remain on the Zoladex if you don't need to be on it, the more likely you are to become androgen resistant, and so the more likely it becomes that you won’t be able to take advantage of this type of treatment when you need it if you were to have metastatic disease.

    Arthur would also note that there may well be good reasons why your doctors think you need to be on the Zoladex, but it is not to “avoid a flare.” It could be because you had high-risk disease to begin with. It could be because you had node-positive disease at the time of surgery. Or it could be for other reasons. Arthur is missing far too much information to have a good understanding of your situation. The problem with staying on long-term androgen deprivation therapy (ADT) of any type is that over time your risk for long-term side effects of such therapy increases and, as already stated, your risk for androgen resistance increases too.

    At present, even if you have developing metastases, you wouldn’t know it because your PSA level isn’t going to go up while you are on the Zoladex unless you become androgen resistant, If that was to happen, and you had metastatic disease, then your PSA would start tio go up pretty fast. You are currently in something of a “Catch 22” situation. The hypothetical advantage of stopping the Zoladex is that you would be able to start it again if your PSA started to rise significantly. If your PSA starts to rise while you are on the Zoladex, then you will be androgen resistant.

  179. Sorry, Arthur — more background …

    I was diagnosed with prostate cancer in late 2012, with a PSA of 24. I was put on bicalutimide for 8 months, then da Vinci surgery at Royal Marsden Hospital in London to remove the prostate and seminal vesicles for locally advanced prostate cancer. Just before the surgery my PSA went up to 37.

    I was put on Zoladex (once every 4 weeks) in May 2014 for an initial run of 2 years.

    Nuclear MRI scans showed that the surgery had not cleared all the cancer, so I had 6.5 weeks of daily IMRT radiotherapy in May-June 2015, also at Royal Marsden.

    As I understand evolution and mutation, when you are on Zoladex the growth of prostate cells is significantly inhibited, until some of the little buggers mutate and become resistant in one of several ways. It’s also my understanding that when you stop the Zoladex, the body compensates soon by boosting testosterone higher and you can get a “flare” of prostate cell growth.

    I would think that any growth like this stands a high chance of producing more mutations, and therefore a higher risk of androgen resistance.

    My question really is, is it possible to have prostate cell growth and metastasis without the PSA showing an increase?


    Arthur responded as follows:

    Dear William:

    Arthur says that clinical trials have shown that in a man like you who shows evidence of remaining cancer after surgery for high-risk disease, the combination of radiation therapy plus 18 months to 3 years of ADT (i.e., with a drug like Zoladex) has the potential — on average — to increase patients’ overall survival compared to just radiation alone or ADT alone. However, individual responses to ADT can vary enormously, and so predicting what will happen to an individual patient is all but impossible.

    When a man is on ADT in a situation like yours, Arthur says we really have no idea to what extent any remaining cancer might be “growing” because the ADT is suppressing the probability of growth. However, it is unlikely that clinically significant growth of a specific tumor is occurring without there being a rise in PSA. What Arthur can’t tell you (and Arthur doesn’t think anyone else can either) is whether the spread of small numbers of cancerous cells (micrometastasis) can continue even while tumor growth is suppressed. And the real question in your case is whether such so-called micrometastasis had already started by the time you had your surgery (especially since your PSA was clearly rising fast at that time).

    Arthur is aware of men like you who are still alive and relatively healthy some 20 years after their initial diagnosis and treatment. He is also aware of men who had far less satisfactory responses to treatment and had died within 5 years of treatmenty. Arthur suggests that the questions that you need to ask your doctors are these:

    (a) How long do you intend to keep me on the ADT before you would be willing to risk taking me off the ADT and seeing what happens (with the understanding that I would go back on if my PSA rose to (say) more than 5 ng/ml within a year after stopping the ADT?

    (b) If I came off the continuous ADT in another 12 months time or so, could we consider some form of intermittent ADT as and when that proved to be wise?

    (c) Given the data from the STAMPEDE trial, is there any justification for trying to consolidate my remission now by using docetaxel-based chemotherapy in addition to the Zoladex?

    It is not necessarily the case that your PSA would rise significantly (what you are referring to as a “flare”, but it would actually be disease progression) if you came off the ADT. That would depend on how well you have responded to the combination of radiation therapy and ADT, and that might depend on where the people at the Royal Marsden thought they could see the continuing presence of cancer on the MRI scans after your initial surgery. It would likely also depend on the aggressiveness of the original cancer (your Gleason score) and any information that the Royal Marsden may have on the genetic subtypes of your cancer.

    Arthur would point our that you clearly started out with a high-risk cancer, and if your Gleason score was 8 to 10 at the time of your surgery, it was a very high-risk cancer. Stopping ADT is always going to come with some degree of risk for such a patient … but staying on the ADT comes with other risks. As Arthur said before, one is therefore in a “Catch 22” situation because if you don’t come off the ADT you’ll never know if you need to stay on it!

    In the interim, Arthur says that if your PSA remains stable and below 0.1 ng/ml it is highly unlikely that there is any significant ongoing disease progression or cancer growth, but it is impossible to know how long you will remain sensitive to the ADT.

  180. Hi Arthur,

    I was diagnosed with prostate cancer with Gleason score of 3 + 4 = 7. My PSA before surgery was 18.9. I underwent RARP (robotic assisted radical prostatectomy) with bilateral extended pelvic lymphadenectomy on 9 November 2015.

    My post-surgery histopathology report states that there is a positive, unifocal, left apical margin. My pathological staging is pT3a: extraprostatic extension.

    My first PSA post-surgery (on 12 December 2015) was 0.037 ng/ml. My subsequent PSA levels have been 0.017 in February, 0.030 in May, and 0.050 in July 2016.

    I want to know if this increase in PSA is normal. Should we wait for another 2 months and monitor it? What is my PSA doubling rate?

    Anil Gupta, MD


    Arthur responded as follows:

    Dear Dr. Gupta:

    Arthur wishes to be very clear that he is not a physician and so he cannot offer you medical advice. However, …

    He says that there are three possible reason why your PSA might be rising like this: (1) There was enough “normal” prostate tissue left behind at the time of surgery for this type of small rise in your PSA to occur, but this situation would need to be monitored carefully to see if your PSA stabilized again soon. (2) The positive apical margin did indeed leave some cancer behind and you will need additional treatment (probably salvage radiation therapy) in the near future. (3) You already had micrometastasis at the time of your surgery, which is a possibility with a Gleason 7 cancer and a diagnostic PSA level of nearly 20 ng/ml (despite your negative lymph nodes and your negative seminal vesicles at the time of surgery).

    The formal definition of biochemical failure after a radical prostatectomy of any type is a PSA level that rises from the nadir level to > 0.2 ng/ml. Your PSA is still well below that level at present. However, the fact that your PSA has risen from a nadir level of 0.017 to 0.050 over a period of just 5 months does seem to suggest the high likelihood of a recurrence of the cancer.

    Arthur would suggest that you could probably wait for one more PSA test to see if your PSA has risen again, but, if it does, then at that point it would seem wise to come to an early decision about salvage treatment. However, this is a decision you need to discuss with your urologist. The hardest question to answer will be whether your rising PSA level is due to the positive apical margin or micrometastasis.

    With respect to your PSA doubling time, we really have no accurate way to assess PSA doubling times in men whose PSA levels are < 0.1 ng/ml. Having said that, it appears to be of the order of about 2 to 3 months, which is really rather faster than one might expect if you just had some normal prostate tissue left behind.

  181. Thank you, Arthur. Very clear and concise information. I decided to stay on ADT Zolodex since this keeps the population down, and restricts growth = cell division = possible mutation = more metastasis. I can deal with the Zolodex for as long as it works. We will keep checking PSA every 2-3 months.

    I have also heard that chloroquine (used for malaria for 100 years) restores the effectiveness of Casodex (bicalutamide), so I have a second-line defense to consider when Zolodex begins to fail.

    Again, thank you


  182. Dear Arthur,

    I was particularly attracted to your conversation with William and appreciate very much your citing the “Catch 22” situation for those of us who are on ADT continuously for 2 to 3 years whilst enjoying peace of mind with undetectable PSA during the treatment period. But not knowing whether the microscopic cancer cells are progressing silently!

    As I have already informed you earlier my case briefly is T2cNoMx, Gleason 9 with positive surgical margins. Treatment: RP + IMRT + Zoladex + Calutide (ADT for 2 years).

    I am very keen to go for the option you have mentioned as (c) STAMPEDE Trial, a systemic and cytotoxic treatment. I will be completing 2 years on Zoladex in December 2016. Up to now my PSA has remained at 0.00 ng/ml throughout ADT whereas my PSA before surgery was 9.7 and before starting any treatment fell to undetectable.

    If I start my third year on ADT with 6 cycles of docetaxel, do you think I am going to suffer unwanted side effects by using chemo upfront or it is more advisable to take a break at the end of 2 years and see what is going to happen to my PSA off ADT? Will there be a difference if I use this option no sooner my PSA reaches 0.1ng/ml off ADT? Should the requirement of the STAMPEDE approach to use docetaxel alongside ADT be at a much earlier stage to get any appreciable benefit?

    You have given a very wide margin for the “Catch 22” guys for their survival: 5 up to 20 years and no doubt, all of us will vote for the double figure!

    Thanks and regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur says that your question is unanswerable for patients like you.

    The data from the STAMPEDE trial shows that the early use of the combination of ADT + docetaxel-based chemotherapy + radiation (in appropriate candidates) extends survival for men who are diagnosed with actual or probable metastatic disease and who are ADT-naive and chemotherapy-naive. You aren’t ADT-naive, and you show no clear indication of metastatic disease, so while we know that docetaxel chemotherapy certainly comes with risks for side effects in men like you, we do not know whether it comes with a potential survival benefit. Furthermore, a trial that could show whether there might be such a benefit in men like you would almost certainly take 10 to 15 years to prove it.

    Arthur thinks that in your situation — subject to discussion with your physicians — the best thing is likely to be to stop the ADT at some point between 2 and 3 years after starting it, and just to see what happens. Your PSA most certainly will rise again after you stop the ADT. The question will be how fast it rises and at what point it will stabilize, but you need to remember that you still have normal prostate cells left in your body, even if all of the prostate cancer cells have been eliminated. As a consequence, those normal prostate calls will make PSA again once you stop the ADT, and so your PSA will rise again, perfectly reasonably, and possibly back up to a level as high as 2.0 to 3.0 ng/ml. When you stop the ADT you need to understand that if you start to “do something” like chemotherapy at a PSA level of 0.1 ng/ml, you won’t have a clue whether you are treating recurrent cancer at all. You will need to wait a lot longer than that to see what happens.

  183. Patrick Turner, 69, here from Australia.

    Sisira has had a couple of good years on ADT, and even with a Gleason 9 tumor. I also had a Gleason 9, T3 diagnosed in December 2009, PSA 5.0, went to 8.0 4 moths later when the doctor could not do an RP after opening me up — too much cancer. So I began ADT, and PSA went to 0.08, then I had a pause for 6 months and PSA went to 8.8, then back to 0.2 nadir. Have been on ADT now for 6 years. Had a 4 month break in 2014, PSA went to 5, then would not drop below 1.0, so the PSA has slowly risen and testosterone suppression with Lucrin has not reduced it enough to get a low PSA. So I had PET scan with gallium-68 PSMA, and I have two metastases in thorax lymph nodes.

    I am the first Australian patient to take part in re-radiation as Dr Gary Shultz has promoted in 2011, with IMRT Calypso. He stipulated patients continue with 150 mg Casudex per day, and have 30 Gy of additional repeated RT. Dr. Schulz claims 45 out of 45 patients became progression-free. That sounds too good to be true. I could not find any supporting scholarly published papers.

    Systemic RT with actinium-225 looks promising but may not be an approved therapy in time for me; I will probably have chemotherapy and salvage ADT anyway. And radiofrequency beacon installation for Calypso left me bleeding for 4 days, then I swam 400 m and I bled again, so maybe I am still bleeding and maybe I cannot do any exercise again, and doctors cannot tell me what they would do if my urethra ruptures or constricts. And incontinence will be sooner rather than later. The ADT has made Rodger shorter, and unable to point, and orgasms are not worth ever trying to have, So that’s OK, there are zero women around feeling frisky at 60, and I don’t expect to ever be touched by any woman ever again.

    My oncologist said there is no cure and all I can do is try to slow down the time between now and being sent up a chimney. I had first round of re-radiation, and in a hospital not run by the government, so there will be a huge expense to try something that maybe only adds month or a year to my life. Some fellows told me their EBRT made prostate cancer vanish for 10 years. But many friends have had RP, and all had prostate cancer return and have had full EBRT to try to fix it. All had complete ED, worse than statistics say, some have incontinence. All are worried, but at least I worry alone without having a partner worry with me because its been 41 years since I became unmarried when she who could not stay vamoosed late one night without saying where, why, or anything.

    So. I like the cafe here with the WiFi, and find pleasure in simple things, and maybe I get to recover a bit, get back onto the bicycle, and back into swimming before being dragged down again.

    Joe Biden was at the opening of a huge, new, 1 billion dollar cancer center in Melbourne yesterday, maybe they can find better ways to defeat cancer.

    All the best to everyone.

  184. Dear Arthur,

    Thank you very much for your wonderful clarification. I will certainly discuss the point you have stressed with my oncologist whether to take the ADT holiday on completion of 2 years or somewhere during the third year. According to the criteria set for the STAMPEDE Trial, I don’t appear to be a suitable candidate and thus feel I should not think of chemotherapy in advance alongside ADT for unproven benefits.

    I was under the impression, after a radical prostatectomy, normal prostate cells will not remain in the body since the entire prostate gland has been removed. I thought the positive margins are all cancer cells and the cells which have possibly migrated out of the prostate gland before surgery too are only cancer cells. Could you please explain to me where I have gone wrong in my thinking? Where do you find the normal prostate cells after the prostatectomy?



    Arthur responded as follows:


    Arthur apologizes. He had forgotten that you had had a radical prostatectomy prior to the radiation therapy, and you didn’t state that in your last message. However, you need to understand that even when one has a radical prostatectomy, there may still be some normal prostate tissue left behind after surgery, and some of this tissue might survive radiation therapy too. All that Arthur is saying is that it shouldn’t be shocking if your PSA rose again a little bit once you stopped the ADT, and you shouldn’t “rush to judgement” if it does start to rise a little because it might stabilize again quite quickly.

  185. Dear Arthur,

    Thank you very much for taking trouble for further clarification.

    If you refer to the beginning of my most recent conversation dated July 17, 2016, in the second paragraph, I have given my case briefly with the treatment received : RP + IMRT + Zoladex + Calutide and also the mention of positive surgical margins. When you answer thousand and one questions, it is quite understandable that you may not remember all what you read from time to time.

    I am now aware my present undetectable level of PSA might show a slight increase before being stabilized once I come off ADT. The problem would be if it shows continuous increases with quicker doubling times with no stabilization at a favourable low level.

    I do not wish to believe the possibility of normal cancer cells remaining after IMRT ajduvant to RP. If so, the more stubborn and aggressive cancer cells will escape the radiation treatment much more easily than normal cells!

    In my case I believe there can’t be any significant influence on the elevation of PSA by any residual benign prostate cells after my radical prostatectomy. I am not quite sure whether microscopic cell leakage applies only to prostate cancer cells and not to the normal cells under any circumstance.

    However, as you always advise me there is no possibility of making accurate comments on the behaviour of microscopic cells counted in millions and billions.

    Many thanks once again.


  186. Dear Arthur,

    Thanks a lot for sharing this valuable information on my current rising PSA level. My urologist has suggested to wait and get a repeat test done after 3 months. But I am very concerned due to my rising PSA and am planning to take a second opinion on my current situation. Can you suggest any good radiation oncologist in the New York/New Jersey/Boston area.

    Anil Gupta, MD


    Arthur responded as follows:

    Dear Dr. Gupta:

    Arthur made it his policy many years ago not to recommend specific, individual clinicians. What he can tell you, however, is that within the New York/New Jersey/Boston corridor you can find literally hundreds of very skilled radiation oncologists who would be well able to discuss your situation with you, and that at almost every one of the major academic medical centers and cancer centers in the region you can find radiation oncologists who specialize almost exclusively in the management of prostate cancer and other genitourinary cancers.

    Getting an early second opinion from a radiation oncologist is certainly not a bad idea. However, Arthur suspects that almost any good radiation oncologist will tell you that he or she would want to see at least one more PSA result before you should be making any decisions about salvage treatment.

  187. Hi Arthur!

    My 4-year anniversary since RP is August 16, 2016. My post-RP Gleason score was 7 (3 + 4) and the only real negative on my pathology report was positive margins at the apex (Gleason pattern 3 at the margins). My last two PSA results (ultrasensitive PSA), 4 months apart, were 0.07 ng/ml; prior to that the results were between 0.04 and 0.05 at 3 months apart for at least over 2 years.

    I assume it is the positive margins that are giving a detectable PSA result. Is it time for salvage radiation, since better results are achieved when the PSA is low or am I overreacting? Don’t want to miss an opportunity for a cure if still possible.


    Arthur responded as follows:

    Dear Mike:

    Arthur says that the question of when to implement salvage radiation therapy when one’s PSA level is as low as yours is a very difficult one. However, if your PSA has only climbed from 0.040 to 0.050 to 0.070 ng/ml over the past 2 years, then your PSA hasn’t even doubled during that 2-year time frame, and a lot of physicians would likely think that it was far too early for you to even consider the need for salvage radiation therapy.

    Arthur would also suggest that it is not necessarily correct to assume that the positive surgical margins are the reason for your rising PSA. You could equally easily have a small amount of non-cancerous prostate tissue left behind that is slowly regrowing, and that may be what is causing your PSA to rise.

    Arthur would encourage you to discuss this situation with your doctors and, at least to agree on some benchmarks that could be used in setting some potential action steps. For example … If your PSA was to rise to 0.100 from 0.070 ng/ml and then from 0.100 to 0.130 at the test after that, at the time of your next two PSA tests, then there might well be good reason to have another talk about salvage therapy, but if Arthur was wearing your shoes at the moment, he would want to be very cautious about initiating what might well be unneeded salvage radiation therapy.

    You also need to consider that the formal definition of PSA failure after first-line surgery is a PSA of 2.00 ng/ml (i.e., about 30 times higher than your current PSA level). If your last two PSA results have both been 0.070, you also need to bear in mind that the next one might come back as 0.060.

  188. Arthur:

    I’ve read a number of questions and your responses to questions concerning the concept of “biochemical failure” following first-line treatment. Is there such a thing as “biochemical failure” following salvage radiation treatments?

    Here’s my story:

    I had robot-assisted prostatectomy in March 2011 at age 62. The surgical pathology reported a Gleason score of 4 + 3 = 7 and noted that the tumor involved 50% of the prostate, was multifocal, bilateral, and present from apex to base. The pathologist noted, “Margins involved by invasive carcinoma, multifocal, right and left posterior lobe. Tumor also comes multifocally within 0.5 mm of the margin.” Lymphovascular and perineural invasion were noted as present and multifocal and the tumor was staged pT3a (extraprostatic extension); the pathologist concluded, “Tumor is focally present in periprostatic adipose tissue at base of prostate and is extensively present within lymphatic and vascular channels in extraprostatic adipose tissue.”

    The first post-surgical PSA in July 2011 was 0.00.

    However, thereafter, the following results were noted:

    03/2012 — 0.12;
    10/2012 — 0.22;
    04/2013 — 0.24;
    10/2013 — 0.43;
    05/2014 — 0.39.

    Then, in November 2014 it doubled to 0.78 and I was referred to a radiation oncologist.

    I received 37 salvage radiation treatments — from early January to March 5, 2015.

    Following salvage radiation, the PSA results were as follows:

    04/23/2015 — 0.79
    10/26/2015 — 0.76
    01/23/2016 — 0.84
    04/20/2016 — 0.67
    07/20/2016 — 1.16

    I was encouraged by the decrease in April, but devastated by the increase that occurred between April and July.

    The urologist is of the opinion that the salvage radiation failed; the radiation oncologist has advised that we cannot make that assumption until we review the results of the next PSA scheduled in October.

    So, what do you make of all this? Is it too soon to conclude that the salvage radiation failed? Assuming there’s a consensus definition of biochemical failure following salvage radiation, do my PSA results support such a finding? Do these post-salvage-radiation PSA results suggest that the cancer has metastasized? Are there any curative therapies remaining? I’ve had scans and MRIs prior to surgery and again prior to the start of the salvage radiation treatments; at what level would you recommend additional scans etc?

    I’ll conclude by noting that I have never experienced any symptoms of prostate cancer. (On the other hand, the treatments have left me incontinent and impotent.)

    Thanks for your help.



    Arthur responded as follows:

    Dear Tom:

    First and foremost, Arthur says that, yes, of course biochemical failure can occur after salvage radiation therapy. However, there is no formal definition of such failure because salvage radiation therapy may be given under such varied circumstances. If we were to apply the Phoenix definition of failure of radiation therapy to your case (which would seem to be reasonable), then biochemical failure would be a rise in the PSA level of 2 ng/ml above the nadir or lowest level achieved after radiotherapy. In your case this would mean biochemical failure when your PSA reached 2.67 ng/ml and was still rising.

    However, … Arthur would also acknowledge that it is equally arguable that in your case biochemical failure occurred when your PSA climbed above the level it had reached at the time of the failure of surgery (i.e., > 0.78), but Arthur would note that it did that; then dropped again; then went up again.

    Under the circumstances, Arthur suspects that both of your doctors are correct in what they are saying: it is likely that you do indeed have biochemical progression after salvage radiation, but that formally you have not actually failed salvage radiation and, because of the well-known occurrence of the “PSA bounce” phenomenon after radiation therapy, waiting to have one more PSA test before doing anything else may well be wise.

    Arthur doesn’t know if this was ever discussed with you, but he is mildly surprised, these days, that you weren’t asked to have a 3 or 4 months of androgen deprivation therapy (ADT, also known as “hormone” therapy) starting a couple of months prior to the radiation therapy as part of the salvage process.

    Arthur says that the question of what to do if your PSA has risen again at the time of your next PSA test is a very complex one that is highly dependent on exactly where the recurrent or remaining cancer is situated. If it was possible to identify that location, then further therapy of various types, targeted to that precise location, might be possible. The obvious problem is that no test to date has been able to identify such a location for you. You might want to ask your doctors whether they think a PET/CT scan of some type might be useful, but the value of PET/CT scanning depends on exactly how it is being done, and most centers with experience of using such a technique (e.g., choline-C11 PET/CT scanning at the Mayo Clinic in Rochester, MN) will only do this on men whose PSA level is > 2 ng/ml because otherwise the risk for false positives and false negatives is too high. If you could get to a center that is carrying out tests using gallium-68 PET/CT scanning, then that might present a better opportunity to identify the location of your recurrence. There is also a newly approved imaging agent called Axumin which can be combined with PET/CT scanning, but again, as yet, this form of imaging appears to be available at very, very few centers.

    Arthur is sorry to hear that you are having to deal with two of the serious side effects of prostate cancer treatment while also having to worry about whether the treatment has even worked.

  189. Patrick Turner here, from Australia.

    I read the post by Tom Senette with interest. In it he says the margins or distance from the tumor to where the surgery begins is extremely small, and it seems there was every chance that surgery did not remove all the prostate cancer cells. But even with wide margins, its highly likely that not all prostate cancer cells are removed, and almost certain a good number of healthy cells remain. Right after surgery, the small numbers of prostate cancer cells, both healthy or cancerous are so small they almost always register an extremely low PSA result, leading many men to breathe a sigh of relief.

    But in all the men I have known who had a radical prostatectomy, all have had “recurrence” i.e., cancer “came back” but of course it didn’t go away anywhere, but whatever prostate cancer cells escaped the surgeon’s scalpel have multiplied enough to give a positive PSA. The healthy survivors of scalpel have same DNA as those of cancer, so they too may well have become cancerous in years following radical prostatecomy. Because the total tumor size is small after radical prostatecomy, there’s more to be worried about after a rising PSA.

    All then men with recurrence had 70 grays of EBRT to the smaller target of surgery site. In all cases, all these fellows had PSA go down and I don’t yet know how all of them are now going. None has had ADT, and this is the “weapon up their sleeve” when cancer laughs at your surgeon and radiation oncologist.

    I have one day left to complete the re-radiation of my prostate cancer after ADT was used in first-line attack on Gleason 9, nine positive samples, aggressive prostate cancer cells, young man’s type, a.k.a. “The Killer”. I call my tumor diagnosed in 2009 “Puff The Magic Prostate Grenade.” Its very likely to explode in a big way and flood my body with metastases, and then I will just have to preside over a slow horrible decline, just like all the other dudes who die from this disease.

    EBRT was in late 2010. It was done because I was in 1% of patients where tumor was so advanced surgery could not be safely done. PSA had only just gone over 5.
    It’s now about 4, has been up to 8 twice, 5.6 again, but ADT is failing. The radiation oncologist in charge of me said I am first in Oz to have had a scan with gallium-68 + CT and PET. This showed two positive lymph nodes in upper thorax plus a “deep blue” prostate gland, but no other metastasis. So these last 3 weeks I’ve had IMRT with Calypso, which also just become available at the Epworth Center in Melbourne. The two spread spots have been done with 45 Gy each, and the prostate gland with 32 Gy, raising total prostate gland level to 102 Gy, which the doctor says is difficult for prostate cancer cells to survive. No drastic side effects at all, so the IMRT plus gel pads to protect rectum damage work real good.

    But I may well find my PSA leaps upwards within 2 months, and I could have radiation-resistant cancer. I will need to accept that chemotherapy will eventually fail, and learn to die in peace with morphine at the end.

    At 69, I still can ride a bike and look after myself real well, better than most other blokes, with a BMI 25, resting heart rate 50, looking good. But ADT and radiation therapy have made Rodger fill up with fibroids; from last year the ED was complete, but continence is still fine. But during this treatment I get up seven times a night to pee, but this will fade to maybe three get ups when swelling recedes after RT. My story is at Patrick’s Concerns at

    Deep realistic thinking is needed about your demise. I don’t hope for a miracle.

    Keep as well as Aunty Destinnee lets you….

    Patrick Turner


    Arthur responded as follows:

    Dear Patrick Turner:

    Arthur is sorry to hear that you were diagnosed with a relatively aggressive form of prostate cancer that was already locally advanced, thus limiting your treatment options at the time of diagnosis.

    You are correct in your opinion that surgery alone would never be a wise treatment option for someone like you, but some of your other statements about the inevitability of progression after surgery in “all” men are simply not borne out by decades of data from tens of thousands of patients. Arthur feels that you need to appreciate that surgery is a highly effective option for some men … but certainly not all of them. If all the men you have known all had recurrences after surgery, that simply tells Arthur that you have met most of those men at the offices of the radiation oncologist who has been treating you. By definition, men who had had first-line surgery and then needed radiation therapy were the ones who had progressed after surgery. Your opinion appears to be the consequence of something known as “selection bias”.

    Arthur would also note two other things. First, that a great deal more than 1% of patients are diagnosed with forms of prostate cancer for which surgery alone would not be a reasonable therapeutic option. Second, that highly aggressive forms of prostate cancer can occur just as easily in older men as they can in younger ones. The idea that highly aggressive forms of prostate cancer are more commonly found in younger men is incorrect. This is another form of statistical misinformation. The vast majority of clinically significant prostate cancers are diagnosed in men > 50 years of age. Thus, when prostate cancer is diagnosed in men who are in their 30s (very, very rare) or their 40s (still relatively rare), it tends to be an aggressive type of prostate cancer and they are often symptomatic at time of diagnosis, but when one does autopsy studies on men in their 30s and 40s who die of other causes (e.g., in car crashes or accidents) a very significant percentage of those men (i.e., 30 to 40%) are found to have small amounts of undiagnosed, relatively low-risk prostate cancer in their prostates at the time of their death.

  190. Dear Arthur,

    I have yet another question for you.

    As you are aware I am taking treatment for my prostate cancer. The cancer status I will mention after I explain to you about my present problem.

    I am suffering (not severely) from three bone issues:

    1. Pain in the right shoulder and fingers in the right hand since 2004. Improved with various treatments taken but not cured. Ignored by me as natural joint pains of old people. No further deterioration and doesn’t look like a big issue.

    2. Same thing happened to my left shoulder and pain and difficulties in movements started since January 20015. During the first few weeks pain radiated all around the shoulder, neck region as well as down the fingers. Some treatments were taken and the condition relieved after a few months and now it is as same as the right shoulder.

    Usually doctors’ explanations on joint pains of the old people are only confusing. They are always some kind of syndrome!

    3. There is pain in my sternum from time to time, developed since March 2016. It does not seem to continue but causes uneasiness from time to time.

    My urologist and the oncologist do not pay much attention when I make such complaints to them since my PSA has remained at zero ever since I started treatment. They are very complacent, and to me it looks like that we have to “live and die by the PSA alone”! Once my oncologist went to the extent of telling me that I should be concerned only if the pains develop in the pelvic and hip region. I think this is not correct since there can be skip metastases which can start secondary tumors in any part of the skeleton or the whole body and I know several survivors of my prostate cancer support group who have been affected by such bone metastasis.

    Yesterday I consulted a senior orthopedic surgeon and sought his advice. He said a MRI scan of both shoulders and the sternum might help to find out what is wrong with these places.

    Though my bone pains are common to old people, I am worried about them because of my cancer situation and wondering whether they could be related to some kind of metastatic disease. Specially 2 and 3 above.

    Now I give below some data which may help you to sort out this problem for me.

    I was diagnosed with aggressive prostate cancer in February 2015. Underwent a radical retropubic prostatectomy in March 2015 (pathology: T2N0Mx; Gleason 9). Adjuvant treatment: IMRT + ADT2. I have been on Zoladex 10.8 mg for the last 15 months.

    During this whole period my PSA has remained at 0.00 ng/ml. The highest level of PSA before surgery was 9.7 ng/ml and 2 weeks after surgery it went down to an undetectable level before any further treatment could start.

    Before the surgery, I was asked to take a whole body bone scan which commented as follows (date: 19.2.2015):

    — Abnormal uptake in the Sternum and T-11 vertebra — Highly suspicious for metastatic disease of bone.
    — Abnormal uptake in bilateral shoulder joints — Degenerative changes most likely

    My urologist said he was very skeptical about the above comments and advised me to get a MRI scan done to evaluate the findings of the bone scan. The MRI report commented as follows after having given a long descriptive analysis (Date: 24.2.2015):

    — Early degenerative spondylosis of the dorsal spine with no evidence of cord or nerve roots compression.
    — The liner hypointensity signal area present across the D-11 vertebra could be an old healed stress fracture too.
    — There is no evidence of marrow infiltrative disease involving the dorsal vertebrae or sternum.

    (I have a feeling the differentiation between metastatic disease and degenerative changes in the spots identified with abnormal uptakes in the bone scan is a mere guess work without any supportive analysis.)

    In the light of the foregoing facts, I would appreciate your views regarding the possibility of drawing any connection with metastatic disease for the bone pains I experience as mentioned in the above three spots. Or are they arthritic or just some other kind of bone issues of the old age unrelated to prostate cancer?

    Thank you in advance.



    Arthur responded as follows:

    Dear Sisira:

    It would be extremely unusual for a man of your age, whose PSA had never gone above 9.7 ng/ml prior to treatment, to have metastatic prostate cancer (even with a Gleason 9 cancer). Could it possibly happen? Yes, it could, but even if it had, it would be highly unlikely to change the way you are being treated at present.

    Arthur tends to agree with your urologist and your medical oncologist about all this. But Arthur is not a doctor and he certainly isn’t a radiologist, and he hasn’t seen your scans, and even if he had seen your scans he couldn’t possibly tell you anything that you haven’t already been told.

    If you really want to spend money having some other form of scan to try and find out whether there is any possibility at all that you have any amount of metastasis anywhere, then ask your doctors if there is somewhere where you might be able to get a gallium-67 PMSA PET/CT scan done in India yet. That is the only current type of scan that even might be able to find such tiny amounts of metastasis. Such scans are available in Germany, but even here in America they are still investigational.

    In all honesty Arthur thinks you are making a mountain out of a molehill with respect to this matter. We all get aches and pains in our shoulders and our hips sometimes as we get older. That doesn’t mean they are associated with what otherwise seems to be a completely controlled prostate cancer. Arthur thinks the only thing that you should really need to worry about at present is if your PSA starts to rise again within the next year or so while you are still on the Zladex and before the doctors tell you that they think you can stop taking the Zoladex. You seem to be forgetting the fact that you have been given potentially curative treatment for your cancer.

  191. Dear Arthur,

    Thanks a lot for your quick response.

    No doubt it is about the best explanation as usual, you have provided for my questions.

    In fact the orthopedic surgeon asked from me the same question whether I am going to change the present treatment regimen in case the MRI or any other test indicates metastasis. I said “No” because I knew even for advanced metastatic prostate cancer with much higher PSA, the starting therapy would be ADT. I have read about the gallium-68 PMSA PET/CT scan and its ability to find very small metastases but again, from a treatment point of view it won’t be of much use in my specific case.

    I will certainly keep in mind all what you have said and specially not forget the idiom “catch 22” as it relates to prostate cancer survivors.

    Many thanks once again.


  192. Dear Arthur,

    I was diagnosed with Gleason 4 + 4 prostate cancer with no mets (PSA at the time was 5.5) in March of 2012. During the last 4 years, I have had a robotic prostatectomy (pathology showed Gleason 4 + 5), salvage radiation, Lupron (end of 2012 and continues today), chemotherapy with Taxotere (as per ASCO recommendation), mets to my iliac bone, radiation to the mets on my iliac bone, and Casodex (am now off because my PSA was/is quickly rising).

    Each treatment initially lowered my PSA (except for the Casodex), but every time it started rising it had a doubling time of 1 month.

    I haven’t been on Xtandi or Zytiga but am a little wary since many cases of aggressive prostate cancer seem to be positive for AR-V7, which has been shown to negate the effects of the two drugs above.

    I had a CT and nuclear bone scan last week and will see my oncologist tomorrow. My mets feel like they have returned and it seems like they are spreading quickly (I feel some pain in my groin and now my lower back).

    So, my question is: Are there diagrams that indicate what treatments are useful at various stages of prostate cancer progression? I know my oncologist uses something, but I would like to see something that will inform me as a patient and the owner of my body.

    Thank you.



    Arthur responded as follows:

    Dear Ted:

    Arthur says that he knows of no formally approved “diagrams” or other formal recommendations regarding the drugs that can or should be used in the treatment of men like you with what appears to be an aggressive form of castration-resistant prostate cancer (whether AR-V7 positive or not).

    Arthur says that there are several drugs that have either been approved by the FDA to treat men in your situation (abiraterone acetate/Zytiga, enzalutamide/Xtandi, docetaxel/Taxotere, cabazitaxel/Jevtana, Xofigo/radium-223, mitoxantrone, and a couple of other, older injectable radiotherapeutic agents) or have been used to treat men like you over the years (ketoconazole, cisplatinum, and others). However, there is no consensus about the “right” or the “best” order in which to use these drugs, in part because we have very limited evidence to show that any of them work really well in cases like yours. Indeed, most reputable organizations state that men like you should be advised to participate in clinical trials of new drug combinations or new drugs in development.

    Arthur is very conscious that this information is not of much help, and that you have probably worked out most of this (if not all of it) out already for yourself.

    What Arthur can tell you is that there is now a test available to identify men who are AR-V7 positive and who are therefore unlikely to benefit from treatment with Zytiga or Xtandi (for detailed information see here).

    Your medical oncologist could be using some sort of guidance given in recent lectures by experts on the management of very late stage prostate cancer. There are several well known specialists who lecture regularly on this topic (Oliver Sartor, MD; Christopher Ryan, MD; Christopher Logothetis, MD; and others) but they all say pretty much the same thing, which is that we have almost no good evidence for the use of the available treatments in any particular order. If Arthur was in your shoes, he would just ask the medical oncologist if you could have a copy of whatever the “guide” is that he is using. One of the problems is that so much depends on the specific mutations that are causing the cancer to progress in specific individuals (AR-V7 is just one among many).

    Another thing that you could do is ask your medical oncologist if he thinks it is worth trying to get a genetic profile done on your tumor cells to see if you have a particular mutation (such as a DNA-repair gene mutation) that might respond to a PARP inhibitor such as olaparib/Lynparza. Lynparza is an approved drug (but it is not yet approved for treatment of prostate cancer) and there are several other PARP inhibitors in development as well. (Click here to see some commentaries on this topic.)

    Arthur hopes that this is at least a little bit helpful.

  193. Dear Arthur:

    I was diagnosed in July (PSA 5.8; Gleason score 3 + 4 in three areas and one 3 + 3 — all on one side of the prostate). I’m really interested in HIFU treatment. I’m trying to get in a clinical trial in Boston but as I started the screening process the funding ran out They are hoping to get funding by October. If this falls through, do you have a recommendation for this procedure outside of the US where the financial burden wouldn’t be as bad? $25k to have this done in Massachusetts.

    Thank you.


    Arthur responded as follows:

    Dear David:

    Arthur is sorry, but he has no information on the pricing of HIFU outside the USA, and $25,000 has been a pretty standard price for HIFU treatment used by all US-based physicians for several years now (when they were actually doing the surgery in places like Mexico and the Caribbean).

    Arthur suspects that your best bet really is still going to be the clinical trial in Boston. However, you might want to note that the most recent data show that both brachytherapy and stereotactic body radiation therapy have been showing pretty good results for men with intermediate-risk disease … but Arthur also recognizes that you are probably trying to avoid either surgery or any type of radiation therapy.

  194. Hi Arthur.

    Could nerve-sparing surgery be a source of PSA because of prostate tissue left behind by the surgeon detectable (0.07 ng/ml)? If so could it cause PSA to increase at a very slow pace? As I mentioned before, I did have a positive margin. My PSA has been between 0.04 and 0.07 ng/ml over the last 2 years?


    Arthur responded as follows:

    Arthur says, “Yes. This is certainly a possibility.”

    However, Arthur would also note that we have no really clear idea to what extent this type of slow PSA rise is really associated with PSA from indolent non-cancerous prostate tissue or from tiny amounts of cancerous prostate tissue that might have been left behind at the type of positive surgical margin you describe. Arthur says that all a patient can really do in a situation like this is to monitor his PSA levels with great care and act swiftly if there is any significant rise in the PSA level indicative of real clinical recurrence.

  195. The problem with radical prostatectomy is that there is a small distance between prostate cells and where the surgical cuts are made so that some prostate gland cells are always left behind after surgery. These may not have any cancer so many men find their PSA falls to < 0.01 after surgery, and they smile, thinking they beat the prostate cancer. But those cells have the same DNA as the prostate cancer cells which are removed, so those remaining cells become cancerous given enough time. I know many men who had radical prostatectomies, then had their PSA rise to just under 1.0 with a rapid doubling time, so they all needed EBRT or IMRT.
    I know one guy who had the Calypso IMRT — the best — 2 years after surgery, and now his PSA is rising again. For the 25% of men who die of prostate cancer, they find its a never-ending battle to their end.

    But one guy who really beat prostate cancer would not have radiation therapy, or a radical prostatectomy, and he had a surgeon remove his bladder, prostate gland, and urethra to Roger off low down. He waved goodbye to his bladder, and to his sex life. His surgeon created a stoma, and he's been fine wearing a urine bag for years now. No more BS from his damn prostate gland.

    Be a real man, and have yourself cut to bits and rearranged, and that's the only reliable way to be sure to beat prostate cancer.

    40,000 people in Australia wear bags for piss or their shit.

    Can't get it up? Use a strap-on vibrator. Or just kiss her nicely, then bring a nice cup of tea to bed, with some candles and Mozart. Learn to give troublesome bits away. Its OK, because I found 99% of females over 55 have zero sex drive. My sister had both breasts removed after finding a small lump. She's well, 5 years later, but has an image problem. Nobody will try anything with her now, at 72. … I'm 69, and had primary EBRT, and later second lot of IMRT, Roger left long ago, and maybe prostate cancer will kill me. Surgeons won't touch me anywhere because I have had radiation, and I piss 15 times a day, shit 6 times, and have become shy because I cannot be where there is no toilet for long.

    I will have to deal with total incontinence due to long-term RT damage.

    Patrick Turner


    Arthur responded as follows:

    Dear Patrick:

    Arthur is sorry that your treatment for your personal and individual case of prostate cancer was so clearly less than completely successful. Arthur also understands your frustration and anger at the consequences. You are far from the only individual for whom prostate cancer has led to such effects. However, since Arthur has no information about your original diagnosis, it is impossible for him to have any idea of whether what has happened to you was predictable (at least to some extent) in any way, shape, or form.

    On the other hand, Arthur would like to note that there are serious factual errors in your comments above. For example:

    — A radical cystoprostatectomy (the removal of the bladder, prostate gland, and urethra all together) can be an effective and appropriate form of treatment for selected men with certain well-defined forms of prostate cancer … but it is not always effective and it is quite certainly not always appropriate or necessary either.
    — You say that “For the 25% of men who die of prostate cancer …”. However, in fact, although the estimated number of new cases of prostate cancer per year in Australia is of the order of 130 per 100,000 men (the same as here in America), only about 26 men in 100,000 are expected to die of prostate cancer in Australia in 2016 (see here to check these facts).
    — Your statement that 99% of women over 55 years of age “have no sex drive” is a very long way off base indeed. It appears that you have been talking to the wrong women.
    — Your statement about the “small distance between prostate cancer cells and where the cuts are made” and your consequent suggestion that it is inevitable that their cancer will recur “given enough time” is simply inaccurate for several reasons. Is it a possibility? Yes it is. Is it inevitable? No. that is not the case.

    Arthur agrees with you that prostate cancer can be a truly horrible disease, and can have effects way beyond those of the cancer itself, as you accurately point out. But it is also important for us all not to exaggerate those outcomes. They lead to unnecessary fears and to over-treatment of many men who can be carefully and appropriately managed with much less aggressive forms of care than you received. On the other hand, Arthur would note that it is certainly true that some men with higher-risk forms of prostate cancer do need aggressive treatment; that a significant percentage of them are not going to be cured by such treatment; and that some of them will have serious complications and side effects from their treatment that they then have to live with for years.

  196. My highest PSA was 37 before DaVinci surgery in November 2013 to remove my prostate and seminal vesicles at the Royal Marsden in London.

    I also had 33 IMRT treatments in the spring of 2015, at the Royal Marsden in Surrey. I have been on Zoladex for 27 months now with PSA showing ~ 0 ng/ml.

    I had Gleason 4 + 3 locally advanced.

    I was on my bike on August 8 and was deliberately attacked by a white van, knocked off bike, hit & run, plenty of witnesses. Police are investigating.

    But I broke my wrist and cracked some ribs. I was in a cast for 6 weeks and the wrist is stiff and sore now, but improving each day.

    My question is: Are metastases more likely at the site of broken bones?




    Arthur responded as follows:

    Dear William:

    Arthur says that that doesn’t sound like a lot of fun!

    Arthur is not aware of any good evidence to suggest that growth of new metastases is necessarily more likely at the sites of broken bones (given the fact that your cancer growth seems to be being successfully repressed by the Zoladex). However, … since bone growth at the site of repair of a fracture is certainly going to be accelerated compared to normal bone turnover, it is certainly a possibility that you should ask your doctors at the Royal Marsden about.

    Arthur also says that you might also want to ask your doctors at the Roayal Marsden whether, given these circumstances, there might be other things you could or should be doing to optimize proper regrowth of the fractures, such as taking calcium tablets and (perhaps) getting at least short-term treatment with a drug like zoledronic acid (Zometa) or denosumab (Xgeva). These are drugs normally used in the treatment of osteoporesis, but the use of one or other of these drugs might also be appropriate in a case like yours.

  197. Hi Arthur,

    After biochemical recurrence (0.2 and rising) is confirmed and it is local (prostate bed or near), will it always spread if there is no secondary treatment or is it possible for the cancer to stay local and not threaten a man’s life? Is there an average PSA level after first-line treatment? Will a man die from his prostate cancer once it has spread if not treated? Does seminal vesicle invasion have a worse prognosis than a positive margin?


    Arthur responded as follows:

    Dear Mike:

    Arthur says that you are asking a series of very simple questions that come with very complex answers, so Arthur will do his best, but the answers to these questions are not “cut and dried”.

    First, Arthur says it is important to understand that risk for progression of prostate cancer after any type of first-line treatment is dependent on way more than just the patient’s PSA level. It can depend on all of the following: his original PSA at diagnosis; the speed with which his PSA is rising at time of progression (either PSA velocity or PSA doubling time); his Gleason score (either at biopsy or better still, after surgery, the pathological Gleason score); his clinical stage at diagnosis, i.e., where the cancer is located (or better still his pathological stage after surgery); and other more esoteric factors like genetic/genomic information.

    Second, with regard to your specific questions:

    — It is theoretically possible that a man who has a rising PSA after treatment with never have metastatic disease and will never die of his cancer, IF he has a Gleason score of 3 + 3 = 6 or less. However, that doesn’t mean that the cancer might not continue to spread locally. It would probably only be wise to just monitor a cancer like this if the patient’s Gleason scoree was 3 + 3 = 6 and his PSA doubling time was at least 2 years or longer.

    — There is no such thing as an “average value” of the PSA level after treatment. That will depend on the patient’s original diagnosis, how he was treated, the success of that treatment, etc. The standard definitions of biochemical success after treatment are: (a) a stable PSA level of < 0.1 ng/ml in a man who has had surgery or (b) a PSA level that drops to a low ("nadir") level in a man who has radiation therapy and then remains stable at a level no higher than that nadir level + 0.2 ng/ml (e.g., from 0.5 to 0.7 ng/ml).

    — The majority of men who have a rising PSA level after first-line treatment and a Gleason score of 3 + 4 = 7 or higher are at significant risk for metastatic prostate cancer and therefore death from that prostate cancer at some point in the future. However, it is very important to understand that the actual risk of dying of prostate cancer is tempered by how fast their disease is progressing (as assessed by their PSA doubling time) and by their actual life expectancy. It could be 5, 10, 15, 20, or even 30+ years away. Thus, for a man with a PSA of 0.5 ng/ml that is doubling only every 18 months, his PSA would probably take 15 years to reach something like 250 ng/ml and he might still have no symptoms of metastatic prostate cancer (although metastasis would almost certainly be visible on a bone scan). However, that man would then be 85 years years of age and therefore would already have been at significant risk of dying of something else in those 15 years based solely on his age.

    — In general, yes, a man who has positive seminal vesicles at the time of surgery is likely to be at higher risk for progression over time than a man who had positive surgical margins. However, that might not be the case if the positive surgical margin was large, if there was more than one positive surgical margin, or if the positive surgical margin involved tissue where the cancer was Gleason pattern 4 or 5.

    The best way for you to be able to evaluate your own personal risk is to use this post-surgical nomogram on the web site of the Memorial Sloan-Kettering Cancer Center. It allows you to enter all of your own personal data and then get projections of your risk at various times after surgical treatment. However, this nomogram will only work reliably if your PSA initially fell to 0.1 ng/ml or less at about 3 months after your initial surgery.

  198. I am 58, good shape, PSA at 40, having gone up from under 2.9 over the last 5 years. Four negative TRUS biopsies and 2 negative MRIs; PCA3 37; 4KScore 31; prostate size 29-30 g. … Urologists can’t explain it and have suggested a RTU of the transition zone or another “random” TRUS biopsy. Why do that if the MRIs cannot even locate a problem? I`m in Mexico and we don`t have “Artemis” here yet to do a MRI/TRUS fusion biopsy. Any thoughts? Similar experiences?

    Thanks in advance.


    Arthur responded as follows:

    Dear Raul:

    Arthur says that this sounds like a distinctly unusual set of circumstances, and that he really has no better idea of what might be going on than the urologists you have already talked with (not that he would expect to anyway). Oh, and he says that for other readers they may need to understand that an “RTU” (or an RTUP) is another abbreviation (in Spanish and in French too Arthur thinks) for what is known as a TURP or transurethral resection of the prostate in English/American.

    Any man with a PSA of 40 ng/ml (up from 2.9 ng/ml within 5 years), a 4KScore of 39%, and a PCA3 score of 39 would normally be expected to have a high-risk and potentially aggressive form of prostate cancer. However, two negative MRIs and four negative TRUS-guided biopsies would appear to contradict the “normalness” of this assumption in your case.

    Arthur would see little point in yet another systematic biopsy at this stage … and it has crossed his mind that what you may really have is some form of mild, chronic prostatitis or even some other rarer form of prostate disorder. This wouid be very unusual but by no means impossible.

    One thing that might help to confirm whether you had prostate cancer or not (and therefore what you might need to do for the long term) would be to talk to one of the urologists you have seen about giving you a single 3- or 4-month shot of androgen deprivation therapy (ADT, also known as “hormone” therapy). If your PSA was to respond to this and drop down to < 0.1 ng/ml, then it would seem very likley that you do indeed have prostate cancer — even if no one has been able to find it. And of course at that point it would still be difficult to know exactly what to do to treat it since we don't know where the cancer is.

    Another possibility is that the amount of cancer in your prostate really is tiny but that the cancer has already metastasized to somewhere else outside your prostate, which is where it is actually growing (which might explain the PSA level and why it has been so hard to actually find the cancer, but again this would be very unusual). Has anyone tried just giving you a bone scan to see if anything shows up outside your prostate?

  199. Dear Arthur:

    Thanks for your response. Now I`m programmed for a choline-11 PET/CT scan to see if there is any cancer inside or outside the prostate (as you mention), any next steps would depend om this result (maybe a fifth biopsy).

    The last four 4 biopsies confirmed an asymptomatic, chronic prostatitis.

    What disconcerts the doctors is the PSA growing so fast. So, no more than wait for the results, keep looking for alternatives, and praying.



    Arthur responded as follows:

    Dear Raul:

    Arthur says it would be unusual, but it is certainly possible that some forms of chronic prostatitis could drive up your PSA this fast.

  200. Dear Arthur,

    Raul’s case appears to be a very rare one and is very interesting to learn about. He seems to have exhausted almost all the tests that could have determined his status. But I don’t see the “color Doppler ultrasound Test” among the diagnostic tests that he has undergone. Could this be of any use at this stage to go for a targeted biopsy?

    Best regards,



    Dear Sisira:

    It seems highly unlikely to Arthur that a color Doppler ultrasound exam would be able to identify a small focus of cancer any better than the type of MRI scan that Raul has already been given.

  201. Dear Arthur:

    Finally we can see the light; the results of the choline-11 PET/CT scan show “positive for the presence of overexpressing tissue of the prostatic membrane upper portion of the left lobe peripheral area with apparent extracapsular spread towards the base of the ipsilateral seminal grandula suggesting tumor activity. No other abnormal areas of radiopharmaceutical concentration suggests tumor activity observed.” (Sorry if it is not the right translation.)

    So you were successful in your thoughts. Now, in a couple of weeks, I’ll have a TRUS biopsy to confirm this and define next steps. According to my doctor, because my age, this could be a TURP + salvage radiation (to be defined).




    Arthur responded:

    Dear Raul:

    Arthur says he is glad to have been able to be of a little help … if only by giving you someone else to “listen”. You seem to have managed to do most of the hard work on your own.

  202. Dear Arthur,

    Most humbly I would like to provide some more information I have on this subject relevant to Raul’s negative biopsies.

    I have a feeling that all the biopsies he has done can be put under the category “blind biopsies” and also there is no indication that he has done DCE-MRI (dynamic contrast enhanced) either. And better still the method combining MRI and advanced Doppler ultrasound technology to produce a three-dimensional “fusion” image that is now being used for performing targeted biopsies using “fusion technology”. An excellent video explaining the method can be viewed at the UCLA web site. This MRI/TRUS-fusion technology is also being used at the LIJ-North Shore Medical System in New York.

    Since of late I have also learned about the availability of the following two advanced diagnostic tests done on prostate biopsy tissues to identify signs of prostate cancer when the visual examinations of the tissues indicate no cancer.

    (1) Prostate Core Mitomic Test: The test can identify prostate cancer by finding aberrations in mitochondrial DNA in cells that is consistent with prostate cancer. The Mitomic test can find molecular markers of cancer. When the Mitomic test is positive for prostate cancer, the finding is accurate 85 to 90% of the time. When the test is negative (finds no cancer) it is accurate 91% of the time. For further information use the web site at

    (2) The ConfirmMDx Test: This test can find genetic markers in these apparently normal cells in the biopsy tissues, suggesting they were near cancer cells in the prostate gland. The test is 90% reliable in determining that a negative biopsy is truly negative, making further biopsies unnecessary and, if confirmed positive, requiring a targeted biopsy to find out the Gleason score of the cancer, etc. For further information use the web site at

    Both these tests are reported to have been tested in studies involving thousands of prostate cancer subjects.

    Reference: Cohen JD. Prostate Cancer Breakthroughs 2014 — Cutting-Edge Diagnostic Tests, New Treatments, Better Options.




    Dear Sisira:

    Arthur says he has no idea whether either of these tests would be available to Raul in South America, but the ConfirmDX test only works in men who have an actual diagnosis of prostate cancer. And, as you will also see, Raul and his doctors seem to have found another way to address his problem.

  203. Dear Arthur:

    Thanks for your answer. No one in Mexico does the TRUS/fusion study yet. There are plans to implement it soon in a hospital in my home town (Artemis). Genetic studies regarding Sisira`s comments only the 4K score and the PCA3 are performed (if we can label those test as “genetic”).



  204. Dear Arthur,

    Sorry I missed your reply. We moved house and both my wife and I had serious surgeries.

    My theory of cancer and Zoladex is evolutionary … that if you restrict growth, you also restrict mutation and, hopefully, metastasis. Simple.

    My oncologist agrees, with awareness of side effects. I tolerate Zoladex pretty well, and I’m on Calci-chew with vitamin D as well now.


    William Donelson


    Arthur responded as follows:

    Dear William:

    Arthur says he hopes you were able to find your prior question and his answer again. You can get to them if you click here.

  205. Dear Arthur,

    I just read your reply to William dated 5th October 2016 by clicking the above link given by you.

    Whilst recommending zoledronic acid for his bone problems, within brackets you have put Zoladex instead of Zometa. I think it has just slipped from your mind, all the words starting with Z. On the other hand I like to read your stuff very carefully although they are not addressed to me because I can learn a lot.

    Thanks and regards,



    Arthur responded as follows:

    Dear Sisira:

    Arthur thanks you for this correction, which the sitemaster has already corrected.

  206. Recently this site listed a discussion about “early cures” (treatments that once worked or were being used in the late 1900s and early 2000s. My search efforts don’t help me find it. Can you? Thanks.



    Arthur responded as follows:

    Dear Bruce:

    Neither Arthur nor the sitemaster is able to remember the discussion abut “early cures” that you are referring to. At Arthur’s request, the sitemaster has looked back at every single post published this year on the site, and even then he was unable to find any such discussion.

    Arthur says that there was a comment a while back about the use of a product call PC-SPES in the 1990s, and the fact that it was specifically associated with prostate cancer-related deaths, even though the people selling it used to claim that it could “cure” prostate cancer. It didn’t.

    In addition, back in 2014 there was this commentary on the use of diethylstilbestrol in the treatment of prostate cancer (which dates back to the 1960s and perhaps earlier).

    Arthur is sorry, but without some more specific information he doesn’t seem to be able to assist you with this question. Is it possible that you saw the article you are interested in on another web site?

  207. Hi Arthur,

    For many men, the after-effects of surgery or radiation treatment (such as incontinence and ED) can be devastating. Do you plan on adding resources on the site to deal with these topics? In particular, options for restoring or compensating for lack of sexual functionality?


    Arthur responded as follows:

    Dear wygk:

    Arthur says that he and the sitemaster have discussed this issue several times in the past. The problem with attempting to add any type of “standard” guidance about how to deal with the side effects and complications of treatment for localized prostate cancer is that almost no form of “standard” guidance works for most men (or for their spouses/partners). There is a very wide range of options that is available. Almost none of them work for “most” men, but on the other hand some of them work extremely well for some subsets of men.

    As a consequence, Arthur says we would have to develop a very wide spectrum of information but then most of it wouldn’t be useful for most readers.

    Arthur would point out that the hardest thing for most men to deal with is not actually the physical problems at all. It is the mental and psychological ones. But it can take many men a very long time to understand that and to realize that they need to change their expectations. However, until they can change their expectations, it may be impossible to resolve the underlying problem.

    Arthur recognizes that this is not a very satisfactory answer to your question, but we have found it easier to suggest to men who have these problems that they join our social network, where they can be talked to one on one as individuals as opposed to being able to just download some information that may not work well for them at all.

  208. Dear Arthur:

    I finally have my results from the 5th biopsy and I share them to you and the group:

    RIGHT PROSTATIC LOBE: Prostatis Chronic / Negative for malignance.

    LEFT PROSTATIC LOBE: Adenocarcinoma acinar little differentiated . Gleason 9 (5+4) or GRADE 5 according to W.H.O.

    SEMINAL VESICLE: Positive for Adenocarcinoma acinar little differentiated

    According to those results, we know this is serious illness and high risk, so, because of my age (58), my Doctor suggests a RRP + SRT in 6-8 weeks.

    I am going to consult a second opinion, but I would like to know yours as well. Best regards.


    Arthur responded as follows:

    Dear Raul:

    Arthur says that even a small amount of Gleason 9 prostate cancer needs to be taken very seriously. However, the question of whether you will need to have the radiation therapy as well as the surgery probably doesn’t need to be determined until after the surgery (because radiation usually isn’t given until several months after the initial surgery). Plenty of men with high-risk prostate cancer like this can be treated effectively with surgery alone. The decision whether the additional radiotherapy is necessary will be easier to make once you have a pathology report after the surgery and if your PSA drops quickly to < 0.1 ng/ml and stays there.

  209. Dear Arthur:

    You are right and I didn`t mention it. Depending on the pathology report of the gland and post-surgery PSA, radiotherapy will be defined after 3 months, approximately, according to my doctor.


  210. On April 17, 2013, my right adrenal gland was removed at Bronx VA hospital. Six weeks later, June 14, my vigorously cancerous prostate was taken out during a 7-hour episode, also done at Bronx VA hospital. In October 2015 a “sling” was implanted with a measure of expectation that the incontinence would improve. During daylight hours I use guards in my jockey shorts and at night, Depends. Before the sling was placed I was up frequently through night time hours. Afterwards and with an adjustment of what I call bladder pills, I am up to urinate an average of two to three times … mostly two. My libido is non-existent. I want to know if I am stuck wearing Depends and having no sex drive for the remainder of my life; I am 72.


    Arthur responded as follows:

    Dear Raymon:

    Arthur says he is sorry but there is no way he can answer a question like yours for an individual patient. The human body is a strange thing, and whether or not your urinary function will continue to improve over time is something you need to discuss with your doctors.

    As for your libido, Arthur says the removal of your adrenal gland will have reduced your ability to make and process androgens, which affect libido. Also, the removal of your prostate will have affected your ability to process testosterone. However, your libido may also have a great deal to do with your age. The libido of most men does start to decline significantly as we get older, but there are exceptions to every rule.

  211. I am not sure if this is how to ask a question, but …

    My husband was diagnosed with advanced prostate cancer 16 months ago. He is on hormone therapy and completed 5 rounds of chemotherapy in February 2016. His cancer had spread to the lymph nodes and bladder. He has problems with urine retention and has had a catheter several times. Had a channel TURP in October 2016 that lasted only a month before he needed a catheter again. He is now due for external radiation treatment and again has a catheter. The radiation oncologist’s nurse says that they can work around that or with it in place. I am wondering about health hazards. I think the catheter is latex. How might that react with radiation treatment?


    Arthur responded as follows:

    Dear Kay:

    Arthur doesn’t claim any great expertise in the technical nuances of radiation therapy, and he really thinks you need to ask that question to the radiation oncologist or the radiation oncology nurse at least. Some forms of “plastic” (and latex is just one form of plastic) are unaffected by low doses of radiation, and so a lot is going to depend on exactly what type of catheter would be in place while your husband had the radiation therapy and what dose of radiation was being given to specific areas of the prostate or simply whether they were going to remove and replace the catheter each time he had the radiation therapy or not (which would be irritating but not actually difficult to do).

    Arthur says you are asking a really good and smart question … and Arthur thinks you get brownie points for asking this. The problem is that Arthur really doesn’t have a good answer for you … but he absolutely does encourage you to call the radiation oncology nurse, tell her your concern, and ask her to explain to you precisely how they would be able to “work around” this problem so that you can feel comfortable that what they say they are going to do really is in your husband’s best interests.

    You are being a good advocate for your husband … and that’s always a good thing — and the right thing to do!

  212. Finally the D day or rather the RPP day is already here (in addition to a lymphadenectomy). Next tuesday I’m scheduled for the Sx PCa; hopefully everything will go OK and by this means I will keep you informed of my progress in recovery. Wish me luck ! Regards from Monterrey, MEX.


    Arthur responded as follows:


    Arthur le desea la mejor de las suertes!

  213. Dear Arthur:

    After 5 days in the hospital, finally at home, only taking antibiotics and pain killers and taking care of the catheter and urine probe. There were more days in the hospital due to a small leak of urine at the urethra. Waiting for the results of the pathology and probably in 2-3 days the catheter will be removed (draining lymphatics fluids). So far so good.

    Regards from Monterrey, MEX


    Arthur responded as follows:

    Arthur hopes you will be fully up and about soon and that your next PSA result is as near to zero as possible!

  214. Dear Arthur:

    I have a question about online nomograms that can be used before surgery to give an idea of the possible extent of disease — for example, the MSKCC nomogram and the Partin tables. It has always been my understanding that if a patient is taking Prosacar or Avodart, the PSA value should be doubled before entering it in these nomograms. But I find it very curious that the instructions on these nomograms make no mention of this. Am I right? Or should one just follow the instructions and enter the PSA value as reported by the lab?


    Arthur responded:

    Dear Tom:

    Arthur says the only people who could answer that question with accuracy are the people who developed them. It is a good question.

    Arthur also says that if he was faced with that question personally (because he was taking dutasetride or finasteride), he would use the nomogram and/or the tables in both the ways you describe. For some men it might not make much difference to the projections. For others it potentially would. Then he would discuss the two different sets of projections with his doctors.

  215. What about green barley pills for high PSA levels?


    Arthur responded as follows:

    Dear Rick:

    Arthur says that this is the first time he has ever heard of the use of green barley pills to manage high PSA levels, and he is aware of no good evidence to support the idea that using this type of supplement on its own could be relied on to have any meaningful effect on either PSA levels or anything else (although, with the assistance of Mr. Google he has quickly been able to find the usual range of miraculous claims that are used to help to sell every supplement under the sun).

    Arthur would point out that “managing” an elevated PSA level is actually not of any clinical value at all because there are all sorts of ways to lower PSA levels temporarily that have little to no effect on the reason that one’s PSA level is elevated in the first place. Having an elevated PSA level is simply a message that there is something not quite right with one’s prostate and/or urinary tract. The degree of “not quite rightness” can vary considerably: from having a slightly enlarged prostate (which is extremely common among men as they get older) to some form of chronic prostatitis (which can be irritating and painful but far from lethal) to a case of metastatic prostate cancer (which might well kill you).

    In Arthur’s opinion, the much more important question is why your PSA level is elevated in the first place. If you know that, then you might be able to decide what (if anything) needs to be done to resolve that problem.

    And having said that, Arthur says that if you like eating green barley pills, they probably aren’t going to do you any harm … but then they probably aren’t going to be doing you much good either. The good that they are doing is most evident in the bank accounts of the people selling these products.

  216. I guess that the main result of taking those pills (green barley) will be go to the WC several times a day without the least effort … LOL!

    Regards from Monterrey, MEX.

  217. Which is better for prostate cancer intermediate IRE or CyberKnife?


    Arthur responded as follows:

    Dear Isin:

    Arthur says that your question is impossible to answer.

    Irreversible electroporation or IRE is a form of treatment for prostate cancer that has been used investigationally in a small number of centers around the world. We have few really good data on the long-term outcomes of men treated for prostate cancer using this technology. By contrast, stereotactic body radiation therapy (SBRT) using CyberKnife technology has been gradually adopted over the past 7 to 10 years and the available outcomes data at about 6 to 7 years of follow-up in several hundred patients now seem to be show a relatively high degree of success. However, …

    Arthur has to point out that the appropriateness of either of these techniques as a treatment for localized prostate cancer in a specific individual patient depends on everything from the patient’s clinical characteristics (age, general health, PSA level, clinical stage, Gleason score, cancer volume, etc.) to the skill and experience of the clinical team that actually carries out the procedure. There is no way that anyone can tell you truthfully that one is “better” than the other for you because the two forms of therapy have never been compared to each other in any type of clinical trial that could provide objective information … and Arthur doesn’t even know if you are an appropriate candidate for either of these procedures. You haven’t provided relevant data. For all Arthur knows, you might be an excellent candidate for simple monitoring on active surveillance …

  218. Arthur,

    I was diagnosed with cT2c, Gleason 4 + 3, PSA 8.8. My treatment of IMRT is just beginning, with neoadjuvant and adjuvant ADT to last a total of 6 months. My first PSA test 2 months in to the first 3-month shot of Lupron had dropped to 0.8. I am concerned that this is not enough of a drop, having read that response to ADT should maybe be less than 0.2, although this seems to be for people who have already had other treatment (surgery or radiation). I have only had 2 of 39 IMRT sessions. Should I be concerned and what should I discuss with my radiation oncologist at our weekly meeting?


    Arthur responded as follows:

    Dear VLH:

    You should discuss this with your radiation oncologist — and perhaps with your urologist too if s/he is the person giving you the Lupron injections — and express your concerns to them. However, …

    You also need to appreciate that what the PSA test actually measures is the amount of PSA that is being released from the prostate into the blood stream, and that is a function of both how much PSA is being produced in the prostate and how much of that PSA is “leaking” out of the prostate and into the blood stream.

    The fact that you have started radiation therapy means that the radiation therapy will be increasing the likelihood that any remaining PSA probably now has an increased potential to leak into the blood stream, so the fact that your PSA has “only” dropped to 0.8 ng/ml may be showing: (a) that the Lupron has significantly lowered your PSA level but that also (b) that the degree of leakage of any remaining PSA into your blood stream has risen.

    Ideally a patient who is on LHRH agonist (e.g., Lupron) therapy will have a PSA that drops to less than 0.1 ng/ml. However, that doesn’t always happen instantly. It may take more than a couple of months. You should ask your doctors whether a PSA of about 0.8 ng/ml is as low as they would expect it to be for someone like you under the current circumstances in their experience.

  219. Thanks, Arthur. The low of 0.8 was measured 2 months into a 3-month Lupron injection and was taken before the IMRT began. This counters the point you made in paragraph 3 — the drop is basically the impact of only the Lupron over 2 months of time. (The shot occurred 2 months after my needle biopsy, so I am assuming any leakage due to that injury to my prostate had ceased.) I will certainly ask my radiation doctor at our next appointment about this and press her to be direct and honest about the degree of drop and what it predicts in terms of the likelihood of curative radiation or issues of micrometastases or other potential problems. (I operate on a hope for the best/prepare for the worst philosophy.)

    If the recommendation is for more than the 6 months of Lupron, not sure what I’ll do. … This drug is not good for quality of life, but neither, I imagine, is metastatic progression to the spine and pelvis.

  220. Hi Arthur.

    Does the Gleason grade at the positive margin play a significant part in whether the cancer progress or not? If a man has localized prostate cancer and his margins were positive after surgery with a Gleason grade of 6 that cancer would not progress as fast as a gGeason 8 at the margins. Correct?


    Arthur responded as follows:

    Dear Mike:

    Arthur says, “Yes”. Your assessment is entirely accurate. A small amount of Gleason 6 disease at a positive surgical margin may be near to irrelevant. A small amount of tissue that is Gleason 8 or higher is a significant (potential) problem.

  221. Hi Arthur!

    If my PSA was 0.047 in 08/2014 and now it is 0.1 as of 04/2017, what is my doubling time within that time frame? The PSA tests were drawn every 3 months using the ultrasensitive PSA test. My surgery was in 2012.


    Arthur responded as follows:

    Dear Mike:

    Arthur says that strictly speaking we have no proven mechanism by which to estimate PSA doubling times in patients whose PSA levels are lower than 0.1 ng/ml, so Arthur can’t say to you that any specific doubling time in the range you are talking about is 100% accurate. However, on a purely mathematical basis, since your PSA has effectively gone from about 0.05 to about 0.10 over 32 months, then it has doubled once in that time frame, giving you an approximate PSA doubling time of … 32 months or nearly 3 years.

  222. If Mike has 12 data points of PSA values (every 3 months for almost 3 years), it’s possible to be much more precise than using only two data points. I’m happy to do the math, if you like; it’s simply (!) curve-fitting to a presumed exponential using a least-squares technique.


    Arthur responded as follows:

    Dear Paul:

    Arthur says that if Mike wants to provide all the detailed data (exact date of each blood draw and exact result of each test), please feel to free to go ahead. However, Arthur’s not sure that the difference is going to be enough to make the work worthwhile. Up to you and Mike if you want to go ahead.

  223. Arthur:

    My last two posts about Gleason grade at the margins and PSA doubling time were basically directed towards me scheduling a consultation with a radiologist about considering salvage radiation. Hopefully it will not come to that. My Gleason grade at the margin (apex) was a 6 and my PSA at this point is moving in the wrong direction — but at a snail’s pace, which is a good thing. Also the doubling time is favorable up to this point. What are some questions to ask the radiologist during my consultation if you can provide any I would appreciate it?


    Thanks for your assistance also sir!


    Arthur responded as follows:

    Dear Mike:

    Arthur thinks that going to talk to a radiation oncologist about the future potential need for salvage radiation therapy is a reasonable idea so long as you are talking to a radiation oncologist who understands that not every patient with a rising PSA necessarily needs salvage radiation therapy — either now or in the future.

    In Arthur’s personal opinion (i.e., if Arthur was in the precise situation you have described for yourself), there are only two really important questions that you need to ask the rad/onc:

    1. “Is there any really good reason why I should even think about having salvage radiation therapy now?”

    2. “What changes in my status would make you think that salvage radiation therapy was wise (in the immediate future or later on)?”

  224. Hi Arthur,

    Thanks for your earlier help. My radiation oncologist is hinting at a 2-year stint on ADT (right now it’s Lupron) following my IMRT/IGRT. I’m currently in the middle of 6 months on Lupron, with radiation having started about 9 weeks into the treatment — and I’m about 40% through the radiation. My disease was first identified at T2a, with 83% positive biopsies, Gleason 4 + 3, PSA 8.8, and suspected extensions; MRI confirmed extensions, and diagnosis was changed to T2c. Scans show no bone or other metastases, no seminal vesicle or lymph node invasion. I am 60 years old, married, and until recently quite happy.

    I am having a hard time on the Lupron. Though I’m a lucky one who has not yet suffered ED and can still, with great effort, have a small orgasm. However, the Lupron is making me feel crazy enough — depressed, hard to sleep, moody, etc. — and is affecting my relationship with my wife (and my “former self”) to a degree that I really wonder what the pros and cons of 2 years are at this point. If 2 years on ADT is going to buy me 2 more years of life, what is the point of that if I spend 2 years on ADT and feel miserable? The oncologist has suggested the possibility of watching for PSA rise and also of intermittent treatment. However, it seems to me that the cancer guidelines just show 6 months ADT plus IMRT/IGRT radiation for T2c. Not sure why she is starting to push for 2 years on this crazy-making drug. I would appreciate your thoughts and what other sources of care I might investigate should she push hard for 2 years on this nasty drug.

    Thanks for any help.


    Arthur responded as follows:

    Dear VLH:

    Arthur wants you to appreciate that there are no “absolute truths” about how long a prostate cancer patient like you should stay on ADT after radiation therapy for an apparent case of localized prostate cancer. In the end this is always a matter for discussion between the individual physician and the individual patient.

    If being on the Lupron is “driving you out of your tiny mind” (so to speak), Arthur says that you basically have two options: (a) simply tell the doctor that you are unwilling to have any more Lupron injections after the initial 6 months or up bec ause of its effects on your overall quality of life; (b) tell the doctor that you won’t take the Lupron for more than 6 months, but you would be willing to talk with her about trying a daily dose of an antiandrogen like bicalutamide (Casodex) after the initial 6 months on Lupron instead.

    Arthur says you also have to bear in mind that no one can tell you with absolute certainty that staying on the Lupron for a total of 2 years will extend your individual life or not. In the end, everyone makes “judgement calls” about how long specific patients need to stay on ADT after radiation therapy — and you need to share your “judgement” with your doctor.

  225. I’m a 58-year-old with low volume, early onset prostate cancer (one sample 5% Gleason 3 + 3, and a secondnd sample 40 percent Gleason 3 + 4, both in left apex area)from a TRUS/mpMRI fusion biopsy. I cannot seem to get a treatment recommendation from an objective doctor that discerns among prostatectomy, radiation, and active surveillance, and mainstream doctors will not even discuss focal laser ablation.

    Seriously, the surgeon recommends surgery, the radiologist recommends radiology, the surveillance oncologist recommends surveillance, and the interventionist recommends interventional ablation. My wife says they are all in sales. SMDH. Any tools or suggestions on how to make this complicated decision would be helpful. Weighing the pros and cons of each treatment, along with the risks of complications, quality of life, longevity of life, feelings about each option, and returning cancer are really mind boggling! HELP! Thanks.


    Arthur responded as follows:

    Dear SteveMc:

    Arthur says that he sympathizes with your situation but that there is no really good answer to your question because you are a perfectly good candidate for a whole spectrum of forms of treatment and the physicians are each telling you that what they know how to do best would work for you (at least for a while). Arthur would point out the following information (which may be helpful, but may well not):

    (1) Arthur says that the key issue regarding active surveillance would be what percentage of the Gleason 3 + 4 = 7 core was actually Gleason pattern 4 (as opposed to Gleason pattern 3). If it is much more than about 1 or 2%, then you might not be able to remain on active surveillance for much more than a year or so.

    (2) Arthur would also point out that even if you were able to have a nerve-sparing radical prostatectomy, the chances are significant that you would not be able to regain the same level of erectile and sexual function as you have currently (even if the operation is carried out by a skilled and experienced surgeon). Recovery of high-quality erectile and sexual function is affected by many things, including your individual anatomy, the precise location of the cancer, and the skill and experience of the surgeon too.

    (3) Focal laser ablation (FLA) is still an investigational technique, and so your insurance is unlikely to cover the cost. That doesn’t mean that it is a “bad” idea, but it does mean that there are very few people who have treated enough patients this way to be really competent at it, and that you would probably have to pay for this out of your own pocket. The outcomes after FLA are also not yet well established. To that extent it is similar to high-intensity focused ultrasound (HIFU) as a treatment for localized prostate cancer.

    (4) You are also a good candidate for almost any type of radiation therapy, and some people would tell you that this is currently as effective as surgery and would leave with good erectile and sexual function (for a while). However, radiation will also affect erectile and sexual function over time.

    Arthur says that the bottom line to all this is that there is no good way to tell you what “the best” form of therapy is for you — and Arthur is utterly objective about this. In the end, this is a judgment call that only you can make (in discussion with your wife, but it is your body so it is your call in the end).

    Much as Arthur would like to be able to give you a simple answer to what you see as a simple question, the problem is that there is no simple answer because actually you are trying to deal with a very complex question.

  226. Arthur:

    Thank you for your reply! I certainly did not mean to imply this is an easy decision, my apologies. Three additional questions please: Would genetic testing the cancer provide more information than is currently known about the aggressiveness of the G4 cancer? My urologist does not think they are worth the expense because there’s is little more information given about the cancer. Is there reason to hope that the current clinical trials on FLA (being done at Maso) will be any more effective in treatment than HIFU, given the use of FLA with a patient saddled inside an mpMRI during treatment? Are there any computerized decision support tools designed for prostate cancer?



    Dear SteveMc:

    Arthur says that there are numerous decision support tools that have been developed to try to help men make decisions about treatment for prostate cancer. The problem is that they really only deal with the “standard” forms of therapy, and (in Arthur’s view) their value is kinda dependent on how much you already know. Since you clearly already know a lot, Arthur is doubtful that any of them would really help you very much.

    Second, there are ongoing clinical trials of FLA at all sorts of places, but as far as Arthur is aware, all of these trials are little more than case series. In other words, there are no randomized trials comparing FLA to something else like HIFU that Arthur is aware of. Arthur is also not aware of what you mean when you refer to “being done at Maso”. Could you have meant Mayo?

    If Arthur was seriously considering FLA, he would go and talk to Dr. Peter Pinto’s group at the NCI Clinical Center in Bethesda, MD. They probably have the best associated imaging group in the country and they have been investigating FLA for years (and the treatment might be free if your insurance doesn’t cover it). There seems to be little doubt that if one is going to have FLA, the best process is when it is done “in bore” with direct MRI guidance so that the treating physician can see exactly what s/he is ablating in real time. There aren’t a lot of places doing this yet. Very few people have treated more than about 50 to 100 patients.

    The problem with genetic/genomic testing is that we have no objective, comparative data to tell us how good any of the genetic/genomic tests are compared to each other or even compared to just knowing the Gleason score and other information. (That is especially the case for anyone with some amount of Gleason pattern 4.) If your insurance will cover the cost, Arthur thinks you should do it, but how much new information it can tell you and your doctors with real accuracy is less than entirely clear.

  227. Yes, I meant Mayo, sorry.

    Thank you again!

  228. Maybe this information could be useful for a better decision making?

    My personal decision-making map (same age as you) was first surgery (RRP in January 2017), depending on the PSA level post-surgery (third month this week) next would be adjuvant or salvage radiotherapy and maybe temporary ADT.

    Regards from Monterrey, MEX

  229. Thank you Raul, very interesting!

  230. I am scheduled to begin a 40 session IMRT program in about 1 month (presently on Lupron and Casodex). My radiation oncologist has “mildly” suggested that before I begin radiation treatment that I consider injection of SpaceOAR Hydrogel between the rectum and prostate to put some distance between them in order to minimize/prevent radiation damage to the rectum (see for a description of the material and procedure). My urologist has similarly given the material/procedure mild endorsement. My question is what can you tell me about the material/procedure so that I may make an informed decision about how to proceed? The manufacturer’s web site has some scary disclaimer language and I have not been able to find out a lot about its efficacy online. I believe it was only FDA approved in 2015. I recently had fiducials, three small metal pellets used for radiation targeting, implanted in my prostate.

    Thanks very much for any information that you can give me.

    Fred, Jr.


    Arthur responded as follows:

    Dear Fred:

    Arthur says that it is impossible for him to tell you whether the SpaceOar procedure is really necessary and a good idea for you in particular. That is really a question for your doctors. What Arthur has been told by the members of the radiation oncology community who have experience with this technology is that it is a good idea for selected patients who may be at higher risk (for any one of several possible reasons) than normal for radiation damage to surrounding tissues during their radiation.

    Arthur would suggest that you read through the two reports on the SpaceOar system written by Allen Edel elsewhere on this web site. The first one was written when the SpaceOar system was first approved by the FDA back in 2015. The second one was written just a few months ago and based on newly reported data about the use of the technology. You may want to note that this technology has been in use in Europe for the best part of 10 years now.

    Are there risks associated with the use of SpaceOar? Yes, there are, and the manufacturer, on its web site, is obliged to make these very clear to you and to physicians. However, as far as Arthur is aware, the actual risk for the individual patient is quite low, especially if the product is being injected by a physician who has appropriate experience with the use of this technology.

    Arthur thinks the bottom line here is that you need to look your doctors in the eye and ask if they really believe you will benefit from the use of this technology and whether the anatomical characteristics of your prostate and the surrounding tissues suggest that you need the additional protection from radiation damage. If they are really only saying “Well, maybe,” then it may not be worth the extra cost and effort, but that’s not something that Arthur can tell you in your particular case.

    Arthur says that you also need to make sure up front that your insurance (Medicare or commercial) is going to cover this additional cost. It is usual for the insurance carrier to request pre-approval for the use of this technology, which your radiation oncologist and his staff would usually handle for you.

  231. I’ve been on Lucrin and Casodex for years.

    I had 70 Gy of normal, four-beam EBRT in 2010 without hydrogel. I bled from the rectum 18 months later, but not large bleed, and like two-thirds of all men getting EBRT. But the EBRT did not kill the prostate cancer and I had 31 Gy IMRT with Calypso as additional radiation therapy to the prostate gland last July in 26 sessions. This slowed the prostate cancer down for about 12 months. But to not damage rectum, I had a hydrogel insert (about 4 mm x 4 mm x 1 mm) between the rectum and the prostate gland, and that prevented the inevitable damage that occurs with radiation therapy to pelvic organs. I did have bad bowel function from a month after radiation therapy but it stopped at 3 months after, and I have no bleeding, so I survived the increase in total radiation to 101 Gy OK. The hospital said the hydrogel cost $2,000, and insertion cost was $500, and I think it ought to be done in all cases where the prostate gland is radiated, or where the prostate cancer begins to grow again in site of surgery after radiation therapy, which is very common! I know so many fellows who had a radical prostatectomy, and then still have had to fight prostate cancer until it kills them. But, …

    Between 2009 to now in 2017, I have cycled 90,000 km on my bicycle, and I am now 70. So despite living with prostate cancer, I have a strong will to live and am now seeking immune therapy. My PSA is at 0.8, has been up to 8.0, Gleason 9, aggressive cells. I want this ahead of dreaded chemo, or theranostics.

    Keep well,

    Patrick Turner
    Canberra, ACT, Australia


    Arthur responded as follows:

    Dear Patrick:

    If Arthur was to choose to have a second round of radiation therapy like you have, after a prior 70 Gy of what sounds like “old-fashioned” 3D conformal beam radiation therapy (3D-CRT) in 2010, he would certainly want to have a hydrogel implant too. However, and with the very greatest respect for your personal opinion, Arthur also thinks we should be clear that men who get first-line radiation therapy with modern IMRT/IGRT today (as opposed to 3D-CRT) do not have anything like the same degree of risk for colorectal complications and side effects (including rectal bleeding) as used to be the case (especially if there is no sign that the cancer is close to the rectal wall). This is one of the primary reasons why most radiation oncologists (who have almost totally converted to the use of IMRT and other forms of image-guided radiation therapy here in the USA) seem to believe that hydrogel implants are not necessarily beneficial for the majority of men being treated this way.

    There are risks associated with the use of hydrogel implants. It is up to each patient, working with his physicians, to come to an individual decision about whether using such an implant is appropriate in his case. Every patient is different and deserves the care and attention that will optimize therapeutic benefit while minimizing therapeutic risk. Arthur is not trained as a physician, and he would never tell a specific patient that he should or should not have a particular type of therapy.

  232. Arthur, thank you very much for your reply and good advice. I will do as you have suggested and ask the questions you have raised.

  233. Patrick: … I neglected to say “thank you” to you for the information that you offered and which prompted Arthur’s comments above. Thank you!

  234. Hi Fred,

    Unless you are one of the few lucky fellows who gets rid of prostate cancer by having a radical prostatectomy, then its very likely to chase you down for the rest of your life. The 10-year stats are probably worse than stated because if prostate cancer spreads to say lungs, and its mutated so there’s no prostate cancer, then cause of death is written down as “lung cancer”, and its not written down as prostate cancer.

    So we have to live awhile with Puff Tha Magic Prostate Grenade, and ya don’t know when it’ll explode. ;-) ?

  235. Dear Mr. Turner:

    It is actually very rare for someone to have metastatic prostate cancer that spreads only to the lungs without also being present in the bones. And the ability to eliminate prostate cancer through a radical prostatectomy is considerable — if it is confined to the prostate, the seminal vesicles, and the immediately surrounding tissues. However, the side effects and complications associated with radical prostatectomy can be significant and should be taken very seriously.

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