Genes, dietary factors, and lifestyle-related factors contribute to the development of prostate cancer. Two inherited susceptibility genes, RNASEL and MSR1, may have roles in responses to infections, raising the possibility that prostate infection or inflammation initiates prostatic carcinogenesis. A new prostate-cancer-precursor lesion, proliferative inflammatory atrophy, may be another link between prostatic inflammation and prostate cancer. Loss of the GSTP1 caretaker function, as cells of proliferative inflammatory atrophy give rise to cells of prostatic intraepithelial neoplasia and to prostate-cancer cells, increases the prostate's vulnerability to genomic damage caused by inflammatory oxidants and dietary carcinogens. Somatic targets of genomic damage include NKX3.1, a candidate gatekeeper gene, as well as PTEN and AR, genes that may modulate the progression of prostate cancer. Inherited polymorphic variants of genes mediating androgen action, AR, CYP17, and SRD5A2, also influence the development and progression of prostate cancer.
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