Targeting prostate cancer based on signal transduction and cell cycle pathways

被引：94

作者：

Lee, John T. ^{[1
]}

Lehmann, Brian D.

Terrian, David M.

Chappell, William H. ^{[1
]}

Stivala, Franca ^{[2
]}

Libra, Massimo ^{[2
]}

Martelli, Alberto M. ^{[3
,4
]}

Steelman, Linda S. ^{[1
]}

McCubrey, James A. ^{[1
]}

机构：

[1] E Carolina Univ, Brody Sch Med, Dept Microbiol & Immunol, Greenville, NC 27858 USA

[2] Univ Catania, Dept Biomed Sci, Catania, Italy

[3] Univ Bologna, Dept Human Anat Sci, Bologna, Italy

[4] IOR, IGM CNR, Bologna, Italy

来源：

CELL CYCLE | 2008年 / 7卷 / 12期

关键词：

radiosensitization; prostate cancer; p53; MDM-2; antagonists; senescence; PTEN; Akt;

D O I：

10.4161/cc.7.12.6166

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：1745 / 1762

页数：18

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