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Prostate Cancer
Volume 2011, Article ID 580318, 12 pages
Review Article

Epigenetics in Prostate Cancer

1Indiana University Melvin and Bren Simon Cancer Center, Indianapolis, Indiana 46202, USA
2Veterans Affairs Medical Center and the Baylor College of Medicine, Houston, TX 77030, USA
3Department of Genitourinary Medical Oncology, M.D. Anderson Cancer Center, Houston, TX 77030, USA
4University of Miami Sylvester Comprehensive Cancer Center, Miami, FL 33136, USA
5Texas Oncology and U.S. Oncology Research, Houston, TX 77060, USA

Received 15 June 2011; Accepted 1 September 2011

Academic Editor: Craig Robson

Copyright © 2011 Costantine Albany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Prostate cancer (PC) is the most commonly diagnosed nonskin malignancy and the second most common cause of cancer death among men in the United States. Epigenetics is the study of heritable changes in gene expression caused by mechanisms other than changes in the underlying DNA sequences. Two common epigenetic mechanisms, DNA methylation and histone modification, have demonstrated critical roles in prostate cancer growth and metastasis. DNA hypermethylation of cytosine-guanine (CpG) rich sequence islands within gene promoter regions is widespread during neoplastic transformation of prostate cells, suggesting that treatment-induced restoration of a “normal” epigenome could be clinically beneficial. Histone modification leads to altered tumor gene function by changing chromosome structure and the level of gene transcription. The reversibility of epigenetic aberrations and restoration of tumor suppression gene function have made them attractive targets for prostate cancer treatment with modulators that demethylate DNA and inhibit histone deacetylases.