Inflammatory processes caused by chemical, physical or biological agents are known to be important cofactors in the pathogenesis of human cancer. In the prostate, epithelial tissue damage followed by cell regeneration in the presence of inflammation is believed to be a key event in neoplastic transformation. According to the ‘injury and regeneration’ model, inflammatory cells infiltrating the prostate release reactive species in response to bacterial/viral infection, uric acid, or dietary prostate carcinogens. Besides inducing inflammation, tissue injury by these and other agents would promote the appearance of proliferative inflammatory atrophy (PIA). A subset of proliferating atrophic cells - possibly showing stem-cell features - may be exposed to the genotoxic insult of free radicals and to an increased rate of mutations and chromosomal aberrations, ultimately leading to neoplastic initiation, promotion and progression. In the last decade, the link between inflammation and cancer and the hypothesis pointing to PIA as a risk lesion for prostate cancer have been extensively investigated at the pre-clinical, clinical, morphological, cellular and molecular levels. In this article, recent reports describing supportive or negative evidence on the link between prostate inflammation, atrophy and cancer are schematically reviewed.

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