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.
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.
Authors: S Hossein Fatemi; Timothy D Folsom; Robert J Rooney; Susumu Mori; Tess E Kornfield; Teri J Reutiman; Rachel E Kneeland; Stephanie B Liesch; Kegang Hua; John Hsu; Divyen H Patel Journal: Neuropharmacology Date: 2011-01-26 Impact factor: 5.250
Authors: Farideh Mehraein-Ghomi; Hirak S Basu; Dawn R Church; F Michael Hoffmann; George Wilding Journal: Cancer Res Date: 2010-05-11 Impact factor: 12.701
Authors: Jan Astermark; Sharyne M Donfield; Edward D Gomperts; John Schwarz; Erika D Menius; Anna Pavlova; Johannes Oldenburg; Bailey Kessing; Donna M DiMichele; Amy D Shapiro; Cheryl A Winkler; Erik Berntorp Journal: Blood Date: 2012-12-06 Impact factor: 22.113
Authors: Gordon A Saxe; Jacqueline M Major; Lindsey Westerberg; Srikrishna Khandrika; Tracy M Downs Journal: Integr Cancer Ther Date: 2008-09 Impact factor: 3.279