Inflammation as a Target for Prostate Cancer Chemoprevention: Pathological and Laboratory Rationale
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Abstract
Purpose:
We review the literature addressing a potential causal role for chronic or recurrent inflammation or infection in the development of prostate cancer.
Materials and 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.
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From the Departments of Pathology and Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, Colorado
© 2004 by American Urological Association, Inc.
