title: Inflammation as a target for prostate cancer chemoprevention: pathological and laboratory rationale.
abstract: OBJECTIVE
  We review the literature addressing a potential causal role for chronic or recurrent inflammation or infection in the development of prostate cancer.
  
  
  METHODS
  A literature search was conducted using MEDLINE to identify articles on chronic inflammation as a risk factor for cancer, particularly prostate cancer.
  
  
  RESULTS
  A causal role for chronic or recurrent inflammation or infection in the development of prostate cancer has yet to be proven. Inflammation may contribute to carcinogenesis by 1 or more of several potentially interrelated mechanisms, including 1) the elaboration of cytokines and growth factors that favor tumor cell growth, 2) induction of cyclooxygenase-2 in macrophages and epithelial cells, and 3) generation of mutagenic reactive oxygen and nitrogen species. Chronic inflammation in the form of stromal and epithelial infiltrates of lymphocytes and histiocytes is extremely common in the peripheral zone of the prostate where most cancers arise. Although differences in histology and terminology exist for these inflammatory and atrophic lesions, as a group they often display evidence of epithelial proliferation. Heterogeneous expression of the GSTP1 gene in such lesions has been proposed as evidence for susceptibility to oxidative damage, thereby providing fertile ground for carcinogenesis.
  
  
  CONCLUSIONS
  Although the cumulative evidence demonstrates that chronic inflammation may be a legitimate target for chemopreventive efforts, more study is needed to prove its etiological role in prostate cancer.
authors.affiliation: Department of Pathology and Preventive Medicine and Biometrics, Unibersity of Colorado Health Sciences Center, Denver, Colorado 80262, USA. scott.lucia@uchsc.edu
authors.forename: M Scott
authors.initials: MS
authors.lastname: Lucia
authors.forename: Kathleen C
authors.initials: KC
authors.lastname: Torkko
mesh_terms: D015984:Causality; D051546:Cyclooxygenase 2; D016207:Cytokines / Q000502:physiology; D004249:DNA Damage / Q000502:physiology; D018450:Disease Progression; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000209:etiology / Q000235:genetics / Q000503:physiopathology* / Q000517:prevention & control*; D026361:Reactive Nitrogen Species / Q000502:physiology; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: D016207:Cytokines; D007527:Isoenzymes; D008565:Membrane Proteins; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases