The convergence of PCA epidemiology, indicating a possible role for prostate inflammation, and a significant role for the diet, in PCA development, with molecular pathology, revealing that neoplastic prostate cells may have acquired an increased vulnerability to carcinogen damage, provides an opportunity for the discovery and development of rational new approaches to PCA prevention. Possible strategies include reduced exposure to genome damaging oxidants and other carcinogens, and intake of antioxidant micronutrients, including vitamin E, selenium, and carotenoids such as lycopene, which may be able to intercept reactive oxygen species before they inflict genome damage in the prostate. Administration of anti-inflammatory agents, when distributed into prostate tissues, may reduce oxidant production by prostate inflammatory cells. Consumption of cruciferous vegetables, containing the isothiocyanate compound, sulforaphane, an inducer of GSTs and other carcinogen-detoxification enzymes, may raise carcinogen defenses in the prostate and in other tissues to compensate for acquired defects in GSTP1 "caretaker" gene function (45-47).
Thus, human PCA itself, featuring ongoing threats to genome integrity associated with prostate inflammation and with high-risk dietary practices, may be the most rational "disease" that needs to be targeted for prevention. To discover and develop new agents to treat prostatic carcinogenesis, new clinical trial strategies featuring new "disease" biomarkers will likely be required. For the near future, the most promising PCA prevention strategies under consideration may be the use of anti-oxidant micronutrients (the SELECT trial) and anti-inflammatory agents (48).
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