Abstract

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• There is emerging evidence that prostate inflammation may contribute to prostatic carcinogenesis. Chronic inflammation has been associated with the development of malignancy in several other organs such as esophagus, stomach, colon, liver and urinary bladder. Inflammation is thought to incite carcinogenesis by causing cell and genome damage, promoting cellular turnover, and creating a tissue microenvironment that can enhance cell replication, angiogenesis and tissue repair. Epidemiological data have correlated prostatitis and sexually transmitted diseases with an increased risk of prostate cancer and intake of anti-inflammatory drugs and antioxidants with a decreased risk. Evidence from genetic and molecular studies also support the hypothesis that prostate inflammation and/or infection may be a cause of prostate cancer. In 1999 De Marzo et al proposed that proliferative inflammatory atrophy (PIA) is a precursor to PIN and cancer. Further research will provide opportunities for the discovery and development of strategies for treatment and prevention of prostate cancer.