Targeting prostate cancer based on signal transduction and cell cycle pathways
Volume 7, Issue 12
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June 15, 2008
Pages 1745 - 1762http://dx.doi.org/10.4161/cc.7.12.6166
Authors: John T. Lee, Brian D. Lehmann, David M. Terrian, William H. Chappell, Franca Stivala, Massimo Libra, Alberto M. Martelli, Linda S. Steelman and James A. McCubrey View affiliations
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.