Prostate cancer is the most common non-skin cancer in the United States, the second leading cause of death from cancer among US men, and the seventh leading cause of death in the United States. The number of new cases of prostate cancer, now estimated at more than 220,000 per year, is expected to increase to more than 380,000 by 2025 because of the aging male population. The incidence of prostate cancer and the rate of death due to the disease increase exponentially with age. The other major risk factors for prostate cancer include a family history of prostate cancer, black race, and a high-fat diet. There is no proven method of prevention. Finasteride inhibits the conversion of testosterone to dihydrotestosterone by the enzyme 5areductase, reducing the level of dihydrotestosterone, the most active androgen in the prostate, by 90 percent. Approved by the Food and Drug Administration as an oral medication for the treatment of symptoms of benign prostatic hyperplasia, finasteride shrinks the prostate by 20 to 30 percent and improves urinary flow rates and symptom scores. In long-term, placebo-controlled trials, finasteride has significantly reduced the risk of acute urinary retention and the need for surgical intervention for benign prostatic hyperplasia from about 10 percent to 5 percent. 1

Because of its beneficial effect on benign prostatic hyperplasia, finasteride was tested, in short-term, placebo-controlled trials, as a treatment for prostate cancer, but it had little effect, reducing serum levels of prostate-specific antigen (PSA) slightly but effecting no commensurate change in the measurable tumor burden. 2 Nevertheless, in the early 1990s, it seemed reasonable to postulate that finasteride might prevent prostate cancer by reducing androgenic stimulation. The Prostate Cancer Prevention Trial (PCPT) was initiated to test this hypothesis