Abstract

PURPOSE:

A new hypothesis for the etiology of prostate cancer is that chronic or recurrent prostate inflammation may initiate and promote prostate cancer development.

MATERIALS AND METHODS:

We reviewed the current direct and indirect evidence from epidemiology, genetics, molecular biology and histopathology implicating inflammation in the pathogenesis of prostate cancer.

RESULTS:

The case for prostate inflammation as a cause of prostate cancer is compelling. Epidemiology data have correlated prostatitis and sexually transmitted infections with increased prostate cancer risk and intake of anti-inflammatory drugs and antioxidants with decreased prostate cancer risk. Genetic studies have identified RNASEL, encoding an interferon inducible ribonuclease, and MSR1, encoding subunits of the macrophage scavenger receptor, as candidate inherited susceptibility genes for familial prostate cancer. Somatic silencing of GSTP1, encoding a glutathione S-transferase capable of defending against oxidant cell and genome damage, has been found in almost all prostate cancer cases. Proliferative inflammatory atrophy lesions containing activated inflammatory cells and proliferating epithelial cells appear likely to be precursors to prostatic intraepithelial neoplasia lesions and prostatic carcinomas.

CONCLUSIONS:

Emerging hints that prostate inflammation may contribute to prostatic carcinogenesis will provide opportunities for the discovery and development of new drugs and strategies for prostate cancer prevention.