Targeting prostate cancer based on signal transduction and cell cycle pathways.
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.
Lee
John T
JT
Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, North Carolina 27858, USA.
Lehmann
Brian D
BD
Terrian
David M
DM
Chappell
William H
WH
Stivala
Franca
F
Libra
Massimo
M
Martelli
Alberto M
AM
Steelman
Linda S
LS
McCubrey
James A
JA
D000970:Antineoplastic Agents / Q000627:therapeutic use; D002277:Carcinoma / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy*; D018797:Cell Cycle Proteins / Q000037:antagonists & inhibitors* / Q000502:physiology; D019008:Drug Resistance, Neoplasm; D006801:Humans; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy*; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors; D015398:Signal Transduction / Q000187:drug effects*; D016159:Tumor Suppressor Protein p53 / Q000037:antagonists & inhibitors
D000970:Antineoplastic Agents; D018797:Cell Cycle Proteins; D016159:Tumor Suppressor Protein p53; D051057:Proto-Oncogene Proteins c-akt