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Review
Targeting prostate cancer based on signal transduction and cell cycle pathways
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
volume 7 | issue 12
15 June 2008Pages: 1745 - 1762
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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.
Authors
John T. Lee
Brody School of Medicine at East Carolina University; Greenville, NC
Brian D. Lehmann
Brody School of Medicine at East Carolina University; Greenville, NC
David M. Terrian
Brody School of Medicine at East Carolina University; Greenville, NC
William H. Chappell
Brody School of Medicine at East Carolina University; Greenville, NC
Franca Stivala
University of Catania; Catania, Italy
Massimo Libra
University of Catania; Catania, Italy
Alberto M. Martelli
University of Bologna; Bologna, Italy
Linda S. Steelman
Brody School of Medicine at East Carolina University; Greenville, NC
James A. McCubrey
Brody School of Medicine at East Carolina University; Greenville, NC









