Abstract
Prostate cancer is the fourth most frequent cancer among men worldwide (40). Given the magnitude of the prostate cancer burden, considerable efforts have been made by the scientific research community to improve our understanding of the factors that contribute to prostate cancer risk and to develop approaches to modify those factors. Age, race, family history, and the presence of certain genetic polymorphisms, all are risk factors for prostate cancer that clearly cannot be modified (13). Prostate cancer incidence increases dramatically with age (46); in the United States, African-American men are at greater risk than whites (46). Heritable effects may account for as much as one-third of prostate cancer risk (1); and genetic polymorphisms in the vitamin D receptor (24,25,52), the androgen receptor (24), N-acetyltransferase (NATI) (16), and certain glutathione S-transferases (GSTs) (45) likely contribute to variations in prostate cancer risk among individuals. Hormones—both sex hormones and insulin-like growth factors (particularly IGF-I)—may also influence the risk of prostate cancer. Evidence indicates that cumulative exposure of the prostate to androgens—including testosterone and dihydrotestosterone (DHT)—contributes to prostate cancer development (9,57).
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