Estrogens and Prostate Carcinogenesis

As summarized earlier, the results of epidemiological studies provide limited evidence for an association between prostate cancer risk and circulating levels of estrogens, which appear to be higher in African American men (under 50 years of age) than in European American men. This observation suggests that estrogens may be involved in prostate carcinogenesis, because men of African descent living in an American environment have the highest risk for prostate cancer world-wide. However, most direct evidence in support for a role of estrogens in prostate carcinogenesis is derived from studies with treatment of NBL rats with testosterone and 17^-estradiol [206,207,244]. The mechanisms involved in the prostatic effects in this model are a mixture of estrogen receptor-mediated and non-receptor processes. In addition, there is evidence to suggest that the mechanisms involved in hormonal induction of rat prostate carcinomas, which originate from the periurethral prostatic ducts, are different from those involved in the induction dysplastic lesions, the dorsolateral prostate acini in this model.

There is evidence for the presence of the CYP19 enzyme aromatase in the human prostate which could provide a local source of estrogens from conversion of testosterone [177-181], but reports are contradictory [182, 183]. The local production of estrogens in the prostate is possibly a stromal process, and stro-mal aromatase activity may increase with aging [184]. Data on the presence of aromatase in the rodent prostate are also somewhat contradictory, because aromatase activity has been reported in the rat ventral prostate and a transplantable rat prostate carcinoma [245] but it was not detectable in mouse prostate [246]. These discrepancies may be due to species or methodological differences.

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