PURPOSE OF REVIEW: Prostate cancer, a common cause of morbidity and mortality in the developed world, ought to be a preventable disease. This review focuses on prostate cancer prevention in the context of new mechanistic insights into human prostatic carcinogenesis. RECENT FINDINGS: Evidence is accumulating to implicate infection and inflammation as contributors to prostate cancer development. Inherited prostate cancer susceptibility genes discovered thus far encode participants in host responses to infection. Proliferative inflammatory atrophy, a prostate cancer precursor lesion, ties inflammatory responses to prostatic carcinogenesis. Somatic epigenetic alterations, present in all prostate cancers, appear to arise in the setting of inflammation. Finally, a newly identified somatic genome change, involving a fusion between an androgen-regulated gene, TMPRSS2, and genes encoding members of the ETS family of transcription factors, may provide a clue as to why prostate cancer cells exhibit androgen dependence for growth and survival. SUMMARY: The contributions of infection and inflammation to the early development of prostate cancer suggest prevention strategies featuring prevention or eradication of infection, amelioration of inflammation, or attenuation of genome-damaging reactive oxygen and nitrogen species. The acquisition of androgen dependence later during prostate cancer pathogenesis suggests the use of approaches targeting androgen signaling, including inhibitors of 5α-reductase.
- Proliferative inflammatory atrophy
- Prostate cancer
ASJC Scopus subject areas