Prostate cancer news reports: Thursday, January 28, 2010

The news reports today cover studies on:

  • Initial PSA levels and risk for prostate cancer in black and in white Americans
  • 3 T MR imaging, MRI-guided biopsies, and identification of sites of local recurrence after first-line EBRT
  • pT0 disease in men with biopsy-detected prostate cancer
  • Outcomes of immediate surgery compared to deferred treatment

Tang et al. set out to test the hypothesis that an initial PSA level greater than the median in men ≤ 50 years of age might predict a different level of risk for prostate cancer among black and white American males. They analyzed data from > 3,500 black and > 6,000 white males, who were divided into groups based on their initial (“screening”) PSA levels as follows: 0.1 to 0.6, 0.7 to 1.4, 1.5 to 2.4, and 2.5 to 4.0 ng/ml. Tang et al. showed that the median PSA level among black and white men was 0.7 ng/ml at age 50 years or less. They also demonstrated that the rate of detection of prostate cancer was not significantly different in the groups with PSA levels of 0.1 to 0.6 and 0.7 to 1.4 ng/ml in black or white men. However, black and white men with initial PSA levels in the 1.5 to 2.4 ng/ml range had a 9.3- and 6.7-fold increase in the age-adjusted risk rate for prostate cancer, respectively. In addition, at up to 9 years of follow-up, an initial PSA level of ≥ 1.5 ng/ml was associated with a gradual increase in the detection of prostate cancer at follow-up in black and in white men. The authors conclude that an initial PSA cutoff of 1.5 ng/ml may be better than a median PSA level of 0.7 ng/ml to determine the risk of prostate cancer in black and white men ≤ 50 years of age.

Yakar et al. have demonstrated the feasibility of using diagnostic 3 T magnetic resonance imaging in conjunction with MRI-guided biopsies to identify the site(s) of local recurrence of prostate cancer after external beam radiation therapy (EBRT). Data was collected from 24 patients who had a rising PSA after EBRT as first-line therapy. Tissue sampling was successful in all 24 patients and in all 38 tumor-suspicious regions (TSRs) based on the initial 3 T MR imaging studies. The positive predictive value  of MRI imaging was 75 percent (15/20) on a per-patient basis and 68 percent (26/38) on a per-TSR basis. The median number of biopsies taken per patient was 3, and the duration of an MRI-guided biopsy session was 31 minutes. Although this technique is apparently feasible, the authors do not address whether this procedure would be either practical or cost-efficient for all patients with a rising PSA post-EBRT.

Bessède et al. have reported on data from 30/7,693 radical prostatectomy cases (0.4 percent) at 6 French centers in which the RP specimens showed no sign of prostate cancer (pT0). Even after careful pathological review, it was clear that cancer was present in at least one of the biopsy cores for each patient, but not in the RP specimen. Patients had received no treatment other that the radical prostatectomy. There are medical-legal ramifications to such cases, but perhaps more interestingly they would seem to confirm the fact that biopsy-detectable prostate cancer can be “managed” (in at least some cases) by the body’s natural processes of self-healing.

Using data from a cohort of patients diagnosed in the Swedish regional component of the European Randomized Screening Study for Prostate Cancer (ERSPC), van den Bergh et al. have shown that, at an average of 5.7 years after initial diagnosis, there was no significant difference in outcomes between patients who received an “immediate” radical prostatectomy (i.e., within an average of 6 months after initial diagnosis) and those who underwent a period of active surveillance and were then treated surgically at an average of 2.6 years after initial diagnosis. It should be noted, however, that the data from this relatively small retrospective database did consistently favor “immediate” treatment.

7 Responses

  1. Re the Swedish ERSPC study above.

    See, this is where us non-scientific types get so confused. The abstract says specifically, as recorded briefly above “… no differences in RP frequencies of Gleason score >6 (odds ratio [OR], 1.54; P = .221), capsular penetration (OR, 2.45; P = .091), positive margins (OR, 1.34; P = .445), RP tumor volume (difference, 0.099; P = .155), or biochemical progression rates (P = .185, P = .689) were found between groups, although all data were in favor of immediate RP.”

    If there are no differences in all measurements, how the heck can the data favor immediate treatment. Talk about Humpty Dumpty being a master of the words and attributing whatever meaning he liked to them!

  2. Re black/white PSA levels:

    O wise one can you interpret this for me:

    “Univariate and age-adjusted multivariate logistic regression was done to estimate the cancer RR in these prostate specific antigen groups. We calculated the prostate cancer rate at subsequent followups.”

    (a) What is cancer RR?
    (b) How do you suppose the prostate cancer rate was ‘calculated’ ?

  3. Cancer RR = cancer recurrence rare = percentage of men with a rising PSA post-treatment.

    With regard to the method of calculation, I am not a statistician. There are standard ways to carry out such calculations, however. The full test of ther paper only states as follows:

    “The chi-square and Mann-Whitney U tests were used as appropriate to compare the PCa incidence in the black vs white groups. Univariate and multivariate logistic regression was done to estimate and compare the PCa RR in various PSA and age adjusted PSA groups. Men with initial PSA less than 0.6 ng/ml served as controls during

  4. Terry: When the authors say “no differences were found,” they mean no statistically significant differences and therefore no specific evidence to support a “real” difference. However, what they are implying by their later statement is that, despite the lack of a statistically significant difference, every result appears to suggest that the patients treated “immediately” had slightly better outcomes numerically — even though the results weren’t statistically significant. In other words, there was a “trend” toward better results in the “immediately” treated patients but it did not reach a statistically reliable level.

  5. Thank you for the explanation of RR — when I grew up that stood for Rhodesian Railways. So, as I understand it the comparison in RR was between ESTIMATES. Hmmmm … given the way estimates are calculated in non-medical arenas, like finance, and their complete and consistent inaccuracy, I guess I migth say I’m not too impressed.

    And I am also grateful for your explanation between a “real difference” and “no difference” — perhaps “unreal difference” might be a better phrase?

  6. The difference between the 2 groups was about 2 years or so of treatment being initialized.

    In my case, at 54 years old at time of diagnosis, I decided that delaying surgery simply mean I would be that much older at whatever time I decided it was right to have the surgery done. Two years older might not normally mean too much, but it is an additional 2 years during which some co-morbidity could enter into the mix. Something totally unforeseen.

    Two years younger might also translate into quicker recovery from the surgery.

    Two years younger might mean less sexual and urological impact from the surgery too.

    Two years younger might translate into less body fat and all of its complications and risk for the surgery. Statistically, men lose muscle mass and gain fat as they age.

    Now, my only personal concern for those 2 years would be denying yourself the possibility of some “break-through” treatment that emerges in those 2 years. I didn’t consider that too likely though.

  7. In my case, also diagnosed at 54, I decided that surgery wasn’t the best option for me at any age. Thirteen years later I still think it was a good decision.

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