Targeting prostate cancer based on signal transduction and cell cycle pathways

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

William H. Chappell (Creator)

John T. Lee (Creator)

Brian D. Lehmann (Creator)

Massimo Libra (Creator)

Alberto M. Martelli (Creator)

James A. McCubrey (Creator)

Linda S. Steelman (Creator)

Franca Stivala (Creator)

David M. Terrian (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: Prostate cancer remains a leading cause of death in men despite increased capacity to diagnose at earlier stages. After prostate cancer has become hormone independent which often occurs after hormonal ablation therapies it is difficult to effectively treat. Prostate cancer may arise from mutations and dysregulation of various genes involved in regulation signal transduction (e.g. PTEN Akt etc. ) and the cell cycle (e.g. p53 p21Cip1 p27Kip1 Rb etc. ). This review focuses on the aberrant interactions of signal transduction and cell cycle genes products and how they can contribute to prostate cancer and alter therapeutic effectiveness. Originally published Cell Cycle Vol. 7 No. 12 June 2008

Additional Information

Publication

Other

Cell Cycle. 7:12(June 2008) p. 1745-1762.

Language: English

Date: 2011

Keywords

radiosensitization, Prostate--Cancer, p53, MDM-2, antagonists, senescence, PTEN, Akt

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