The Saturday prostate cancer news: November 29, 2008

We have separately addressed a report on 10-year outcome data following (non-robotic) laparoscopic radical prostatectomy for localized prostate cancer. In today’s other reports we have addressed:

  • The potential of annexin A3 as a marker for early diagnosis of prostate cancer
  • The ability of PSAV and PSAD to predict risk for prostate cancer in men with one or more negative prostate biopsies
  • Estrogens, estrogen receptors, and prostate cancer development and progression
  • Differences between clinical and pathological Gleason scores and the impact on outcomes following surgery

Schostak et al. have identified the urine level of annexin A3 as a highly specific, non-invasive marker for early detection of prostate cancer. They have also shown that the combination of annexin A3 level in urine and total serum PSA level is superior to any other combination of annexin A3 with percent free, complexed, and percent complexed PSA level in predicting the likelihood of a biopsy that is positive for prostate cancer. The authors suggest that the combination of annexin A3 level in urine and total serum PSA level has “huge potential to avoid unnecessary biopsies,” particularly among those men with a negative DRE and a PSA level between 2 and 10 ng/ml.

In a study from Spain, Rodríguez Alonso et al. have reported on the relationship between PSA density (PSAD), PSA velocity (PSAV), and prostate cancer for men with one or more negative prostate biopsy results being (presumably) treated for symptoms of benign prostatic hyperplasia (BPH) with transurethral resection of the prostate (TURP) or radical prostatectomy. According to their data, prostate cancer was identified in 16/170 patients (9.4 percent). Both PSAD and PSAV were specifically predictive of risk for prostate cancer in these 16 men, and the most sensitive PSAD and PSAV cut-off points in detecting prostate cancer were 0.15 ng/ml/cm3 and 1 ng/ml/year, respectively.

Bonkhoff and Berges have reviewed available data on the mechanisms of action by which estrogens may affect prostate carcinogenesis and prostate cancer progression. The human prostate is equipped with two types of estrogen receptor: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). This estrogen receptor system undergoes profound remodeling during development and progression of prostate cancer. Noting that estrogens have been used to treat advanced prostate cancer for > 60 years, Bonkhoff and Berges point out that (paradoxically) estrogens may also be involved in the development and progression of prostate cancer. Recent data have suggested that ERα may be a promising target for prostate cancer prevention, and that ERβ may act as a tumor suppressor.

The fact that there are often differences between the clinical Gleason score determined at biopsy and the pathological Gleason score detrmined after radical prostatectomy is well known. Boorjian et al., using data from the the extensive Mayo Clinic surgical series, have now demonstrated that: (a) biopsy Gleason score was significantly associated with systemic progression in patients with pathological 3 + 4 and 8 to 10 cancers; (b) biopsy Gleason score was an independent predictor of death from prostate cancer in patients with pathological Gleason 3 + 4 tumors; but that (c) adding the biopsy Gleason score to the pathological Gleason score, PSA level, and seminal vesicle and margin status did little to increase the predictive value of the current Mayo Clinic prognostic model, which already emphasizes the relative importance of pathological criteria for risk stratification.

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