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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 2008
Pages: 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


Purchase article for $19

Subscribe to this journal for $129/year