What did we learn at the AUA this year?


The annual meeting of the American Urological Association (AUA) is one at which a great deal of information is exchanged, but a lot of that information is of limited utility to patients. Why? Because the information is often of an incredibly detailed nature and relates to the precise ways that diagnosis, prognosis, and treatment for prostate cancer are carried out and is not really very “generalizable” for the “average” patient.

However, this does not mean that there aren’t interesting and useful “nuggets” of knowledge that we take away from the meeting each time we attend. So, …

Here are the five key pieces of knowledge that your sitemaster took away from this year’s meeting in Chicago over the 3 days from Friday though Sunday:

  • The so-called PREDICT Prostate prognostic tool — developed in the UK on the basis of data from the ProtecT trial (and which we first referred to in March this year) — has been re-validated using data from > 69,000 men in the nation-wide, population-based Prostate Cancer data Base Sweden (PCBase). This re-validation (see here for more details) appears to confirm the accuracy of the PREDICT Prostate nomogram with a high degree of accuracy and reproducibility for men initially diagnosed with localized (i.e., non-metastatic) forms of prostate cancer.
  • The precise value of MRI scanning in the diagnosis and monitoring of men with localized forms of prostate cancer remains controversial, as does the role of targeted biopsies using MRI guidance. Numerous presentations on these and related topics provided conflicting sets of data and information. It is increasingly clear to your sitemaster that the value of MRI-generated information is highly operator-dependent, and involves both the quality of the actual MRI itself and the quality of the evaluation and interpretation of the consequent imagery. This is not to say that MRI scans prior to certain types of biopsy aren’t useful. They are. However, the degree of usefulness is inconsistent. If your sitemaster was placed in the position where an MRI (and a consequent MRI/TRUS fusion-guided biopsy) was considered to be a good idea, he would want to make absolutely sure that both the MRI itself and the consequent fusion biopsy were being carried out at centers with very high levels of experience and expertise.
  • The associated corollary to the last bullet point is that assignments of PI-RADs scores based on MRI scanning data cannot always be relied on. In other words, it cannot necessarily be assumed that a man with a PI-RADs score of 1 has low-risk prostate cancer or that a man with a PI-RADs score of 5 has a high-risk prostate cancer. Cases being presented at the AUA clearly demonstrated the existence of “MRI-invisible” prostate cancer tumors at one end of the scale and “MRI-positive” tissues with PI-RADs scores of 5 that turned out not to be prostate cancer at all.
  • One leading prostate cancer expert advised your sitemaster that at his center no one was being put on active surveillance any more until they had had a genomic test (e.g., an Oncotype DX or Decipher test) demonstrating that they were at low biological risk for disease progression — whether their Gleason scores were low-risk (3 + 3 = 6) or favorable, intermediate risk (3 + 4 = 7). This particular center has now come to the conclusion that such objective data (as opposed to operator-dependent data like histopathology slides and MRI scans) are more accurate at prediction of risk for progression over time, and therefore more helpful at determining who is and who is not a good candidate for active surveillance. However, we do not, as yet have any confirmation of this particular belief from any type of clinical trial. If this were to turn out to be true, such data would clearly need to be integrated into the PREDICT Prostate nomogram above-mentioned.
  • Finally, there was one poster at the AUA that suggested the possibility that an old drug used in the treatment of cardiovascular conditions like hypertension and angina — atenolol — might have utility not only in the prevention of localized prostate cancer but also in the prevention of the progression of prostate cancer for men on active surveillance or even for men who received first-line treatment for some forms of clinically significant, localized prostate cancer. We should emphasize, however, that a lot of work would still need to be done to validate this hypothesis. We are absolutely not suggesting that men on active surveillance or anyone else should be treated with atenolol to prevent or delay progression of prostate cancer at the present time outside of a well-structured and IRB-approved clinical trial

4 Responses

  1. Thank you for the recent AUA highlight review. Your personal thoughts on various topics are right on and readers would be wise to utilize them in their planning.

    One topic that caught my attention was the subject of prostate cancer tissue biomarkers and their use. You mentioned one outside opinion which you questioned (thank you), but there have been a couple of recent reports to suggest these biomarkers are virtually worthless because they are not giving you the worst case scenario of the prostate cancer you have due to sampling error. For the test to be useful, one would have to sample all the areas of PCa and run the test on the most high risk area. Perhaps, someone will eventually do that on whole mount specimens, but right now what we are getting is an average reading which may not sufficiently alert one to a problem.

    One is reminded of a single case where they genetically analyzed a deceased person’s the prostate cancer of a man who had died from prostate cancer.The source of the prostate cancer that metastasized and killed the person was a little area in the prostate; it was not the dominant prostate lesion. This illustrates how difficult this is.

  2. For interested, nerdy readers, here is a discussion from NCI/NIH of AI and machine learning to increase accuracy of mpMRI and reduce interobserver variability of PI-RADs scoring:

    Work on initial detection using imaging continues with biparametric MRIs, hyperpolarized [13C]pyruvate MRIs, RSI-MRIs, and advanced PET scans.

  3. Dear Walter:

    I actually had also asked the specialist very specifically about the issue that you raise. He told me that there had been occasions when a patient had two apparently different significant lesions on biopsy and he had specifically asked the genetic testing company to test tissue from both sets of cores for exactly the reason you are referring to. However, he felt very comfortable that, in a very high percentage of cases, if tissue from the index lesion is the tissue tested, one is going to get a result with a high probability of accuracy. BUT …

    He and I both agreed that no one test is or can be the be all and end all of these decisions. Physicians should be taking all relevant information into account in making recommendations to patients: clinical stage, Gleason score or grade group, PSA level, MRI and TRUS data, symptomatology, family history, etc., etc. It is simply not possible to be 100% accurate 100% of the time — and it probably never will be.

    What is more, it is always easy to find the exceptions to general rules because people go looking for them. I am pretty sure that the single case you are referring to is the one patient in the entire John Hopkins series of 18,000 or so patients where they found — post mortem — that a patient who had been diagnosed with Gleason 6 disease on biopsy and was confirmed to have Gleason 6 pathologically after a radical prostatectomy actually had a submicroscopic amount of Gleason 7 disease.

    This will happen again in the future. It is inevitable.

  4. Prostate MRI has only moderate interobserver agreement, even amongst experts. I had the prostate MRI read as both a PI-RADs 3 and PI-RADs 2 read by radiologists at nationally known cancer centers.

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