Finasteride and prostate cancer.

Abstract

Although testosterone is the major circulating androgen in men, dihydrotestosterone (DHT) is more potent and is the major form of androgen found within the prostate gland.1 DHT, which is responsible for maintaining prostate growth, is produced through reduction of testosterone by an enzyme called 5-α-reductase.1 DHT is regarded as an extremely important factor in the pathogenesis of benign prostatic hyperplasia (BPH).2 There are 2 isoforms of 5-α-reductase (types 1 and 2). The type 2 enzyme predominates within the prostate and is localized to the fibromuscular stromal compartment.3 Therefore, finasteride, a selective competitive inhibitor of 5-α-reductase type 2, was developed to address the management of BPH.4 Accordingly, use of finasteride significantly reduces urinary symptom score, improves urinary flow rates, and reduces prostate volume in men with BPH.2 Like BPH, prostate cancer is known to be androgen-dependent, and finasteride inhibits the proliferation of prostate cancer cell lines both in vitro and in vivo.5,6 These findings incited the National Cancer Institute (NCI) and the South West Oncology Group (SWOG) to consider whether finasteride could reduce the risk of prostate cancer. In 1993, a large-scale study of prostate adenocarcinoma chemoprevention with finasteride was initiated: the Prostate Cancer Prevention Trial (PCPT). A recently published paper reports the findings of this important study.