Urologic Oncology: Seminars and Original Investigations
Volume 24, Issue 2 , Pages 152-160, March 2006

The application of epigenetic modifiers on the treatment of prostate and bladder cancer

  • Zhengwang Zhang, M.D., Ph.D.

      Affiliations

    • Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9110, USA
  • ,
  • Jose Karam, M.D.

      Affiliations

    • Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9110, USA
  • ,
  • Eugene Frenkel, M.D.

      Affiliations

    • Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390-9110, USA
  • ,
  • Arthur Sagalowsky, M.D.

      Affiliations

    • Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9110, USA
  • ,
  • Jer-Tsong Hsieh, Ph.D.

      Affiliations

    • Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9110, USA
    • Corresponding Author InformationCorresponding author. Tel.: +1-214-648-3988; fax: +1-214-648-8786

Abstract 

Prostate cancer and transitional cell carcinoma (TCC) of bladder are the 2 most common malignancies in the male adult urogenital system. Epigenetic gene silencing, particularly tumor suppressor genes, has become a new area of cancer research. Agents such as deoxyribonucleic acid methyltransferase inhibitors or histone deacetylase inhibitors are epigenetic modifiers that can restore gene expression and alter the malignant phenotype of cancer. They provide a new therapeutic avenue for prostate cancer and TCC. It is also likely that combination regimens using epigenetic modifiers with other classes of agents may have higher therapeutic efficacy for prostate cancer and TCC, especially metastatic and/or refractory cases. We review current knowledge of epigenetic event in prostate cancer and TCC, and discuss the possible clinical implications for these 2 diseases.

Keywords:  Epigenetics , Prostate cancer , Bladder cancer , Histone deacetylase , Deoxyribonucleic acid methyltransferase

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 This work was supported by a United States Army grant (DAMD17-03-2-0033 and W81XWH-04-1-0222) and the National Institutes of Health (CA95730).

PII: S1078-1439(05)00265-6

doi:10.1016/j.urolonc.2005.11.004

Urologic Oncology: Seminars and Original Investigations
Volume 24, Issue 2 , Pages 152-160, March 2006