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World J Clin Oncol. Feb 10, 2013; 4(1): 4-13
Published online Feb 10, 2013. doi: 10.5306/wjco.v4.i1.4
Development of animal models underlining mechanistic connections between prostate inflammation and cancer
Murielle Mimeault, Surinder K Batra
Murielle Mimeault, Surinder K Batra, Department of Biochemistry and Molecular Biology, College of Medicine, Eppley Cancer Institute, University of Nebraska Medical Center, Omaha, NE 68198-5870, United States
Author contributions: Mimeault M searched and reviewed the literature and wrote the manuscript; Batra SK reviewed the literature and revised the manuscript; Both authors read and approved the final version of manuscript.
Supported by In Part by the National Institutes of Health National Cancer Institute, R01CA138791
Correspondence to: Murielle Mimeault, PhD, Department of Biochemistry and Molecular Biology, College of Medicine, Eppley Cancer Institute, University of Nebraska, Medical Center, Omaha, NE 68198-5870, United States. mmimeault@unmc.edu
Telephone: +1-402-5595455 Fax: +1-402-5596650
Received: January 1, 2013
Revised: January 29, 2013
Accepted: February 7, 2013
Published online: February 10, 2013
Processing time: 78 Days and 0.3 Hours
Abstract

The characterization of animal models has indicated that the genetic, dietary and environmental factors and hormonal imbalance may influence the risk to develop prostate inflammatory lesions and prostate cancer (PC) confirming human epidemiologic data. It is now established that the prostate inflammatory response typically results in major changes in the local microenvironment of epithelial cells of the prostate gland, including an intense stromal remodeling, activation of fibroblasts, infiltration of immune cells such as mast cells, macrophages and B and T lymphocytes and collagen deposition. The immune cells recruited at prostate inflammatory lesions and myofibroblasts may contribute to the release of numerous pro-inflammatory cytokines and chemokines that in turn can promote the oxidative stress, genomic instability and proliferation of epithelial cells. The accumulation of additional genetic and/or epigenetic alterations in prostatic stem/progenitor cells may subsequently culminate to their malignant transformation and PC initiation and progression and more particularly with advancing age. The potential mechanistic relationships between the molecular events associated with the persistent inflammatory response and prostate carcinogenesis have important implications for optimizing the current therapies against different prostatic disorders and PCs.

Keywords: Animal models; Prostate inflammation; Tumor microenvironment; Stromal remodeling; Prostate cancer; Therapies