In an article in the August 10th issue, NCI Director Andrew von Eschenbach, MD, when asked if the Prostate Cancer Prevention Trial (PCPT) had sent some mixed cancer prevention messages to the public, since men in the study who did develop prostate cancer while on finasteride (Proscar/Propecia) were more likely to have higher-grade tumors, responded, “Cancer is a very complex problem; the science coming from studies is complex” (“IOM Report: 60,000 Cancer Deaths Could Be Prevented Yearly with Current Knowledge,” p 6).
The genetic, biochemical, epidemiological, experimental, and clinical reasons for my warnings1-4three years ago that finasteride promotes prostate cancer have been confirmed by the findings of the finasteride chemoprevention trials (PCPT) involving 18, 882 men followed for seven years. The trial was stopped after 9,060 men were biopsied during the trial or at the end of the trial of seven years.
“Finasteride prevents or delays the appearance of prostate cancer…” by 24.6% (finasteride 803/4368 [18.4%] vs placebo 1147/4692 [24.4%]) but increased the risk of high-grade prostate cancer (Grade 7, 8, 9, 10) by 67% (finasteride 280/757 [37%] vs placebo 237/1068 [22.2%] [p<0.001]).
The Data and Safety Committee terminated the trial because of the increased risk factor of 1.7 for high-grade tumors among those in whom prostate cancer was detected.5
The “End of Study” biopsies of the men who were not biopsied during the seven years (no PSA > 4.0 ng/ml, no induration on digital rectal examination (DRE), no urinary retention) showed a 60% increase in high-grade prostate cancer (finasteride 92/364 [25.3%] vs placebo 89/564 [15.8%] [p<0.001]). Even with intensive screening high-grade prostate cancer was promoted without warning by finasteride.
The Phase I trials of finasteride showed that finasteride at 1 mg (Propecia) blocked 5 alpha reductase as well as finasteride at 5 mg (Proscar).
The suggestion by Dr. Peter Scardino noted in the OT article on the study in the July 25th issue and in his NEJM Editorial that young men (younger than 35) might have the “added benefit of cancer prevention” is not correct, as these men will have added risk for promoting high-grade prostate cancer for over 50 years.
In a 2000 letter in the Journal of Urology, the PCPT principal investigators, Ian M. Thompson, MD, and Charles A. Coltman, MD, state “…that the only way to reach a conclusion [re: finasteride promotion of prostate cancer] is not through speculation but through hard work in clinical trials. We look forward to reporting these results in another four years.6
The PCPT trial was stopped after three years in March 2003 because finasteride promoted high-grade prostate cancer as I had predicted (“speculated”).
W. Reid Pitts, Jr., MD
Associate Clinical Professor (Urology) New York Presbyterian/Weill Cornell Medical College New York City
1. Pitts Jr WR. Letter Re Chemoprevention of urological cancer. J Urol 2000;163:1260–1261.
2. Pitts Jr WR. Letter Re Back to the future-the role of complementary medicine in urology. J Urol 2000;164:461.
3. Pitts Jr WR. Reply to critique of “Chemoprevention of urological cancer” J Urol 2000;164:1332.
4. Pitts Jr WR. Prostatic intraepithelial neoplasia and putative precursor lesions of prostate cancer: a clinical perspective. BJU International 2001;88:985–986.
5. Thompson IM et al: The influence of finasteride on the development of prostate cancer. N Engl J Med 2003;349:213–222, Table 5.
6. Thompson IM, Coltman CA. Re: Chemoprevention of urological cancer, letter. J Urol 2000;164:1321–1322.