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Brian Lehmann
Last active: 9/15/2015

Targeting prostate cancer based on signal transduction and cell cycle pathways.

Lee JT, Lehmann BD, Terrian DM, Chappell WH, Stivala F, Libra M, Martelli AM, Steelman LS, McCubrey JA
Cell Cycle. 2008 7 (12): 1745-62

PMID: 18594202 · PMCID: PMC2593475 · DOI:10.4161/cc.7.12.6166

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, p21(Cip1), p27(Kip1), 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.

MeSH Terms (11)

Antineoplastic Agents Carcinoma Cell Cycle Proteins Drug Resistance, Neoplasm Humans Male MAP Kinase Signaling System Prostatic Neoplasms Proto-Oncogene Proteins c-akt Signal Transduction Tumor Suppressor Protein p53

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