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