Lee, John T.Lehmann, Brian D.Terrian, David M.Chappell, William H.Stivala, FrancaLibra, MassimoMartelli, Alberto M.Steelman, Linda S.McCubrey, James A.2011-04-152011-05-172011-04-152011-05-172008-06-15Cell Cycle; 7:12 p. 1745-1762http://hdl.handle.net/10342/3339Prostate 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 2008en-USAuthor notified of opt-out rights by Cammie Jennings prior to upload of this article.RadiosensitizationProstate--Cancerp53MDM-2AntagonistsSenescencePTENAktArticlePMC2593475