Published in

Taylor and Francis Group, Cell Cycle, 12(7), p. 1745-1762

DOI: 10.4161/cc.7.12.6166

Links

Tools

Export citation

Search in Google Scholar

Targeting prostate cancer based on signal transduction and cell cycle pathways

Journal article published in 2008 by John T. Lee, Brian D. Lehmann, David M. Terrian, William H. Chappell, Franca Stivala, Massimo Libra ORCID, Alberto M. Martelli, at East Carolina University Nc Docks, Linda S. Steelman, James A. McCubrey ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Red circle
Preprint: archiving forbidden
Orange circle
Postprint: archiving restricted
Upload
Red circle
Published version: archiving forbidden
Policy details
Data provided by SHERPA/RoMEO

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. Originally published Cell Cycle, Vol. 7, No. 12, June 2008