Akt-regulated pathways in prostate cancer

被引：291

作者：

Majumder, PK

Sellers, WR

机构：

[1] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA

[2] Brigham & Womens Hosp, Dept Internal Med, Boston, MA 02115 USA

[3] Harvard Univ, Sch Med, Boston, MA 02115 USA

[4] Harvard Univ, Broad Inst, Cambridge, MA 02141 USA

[5] MIT, Cambridge, MA 02141 USA

来源：

ONCOGENE | 2005年 / 24卷 / 50期

关键词：

PTEN; AKT; prostate cancer; phosphoinostide; 3-kinase;

D O I：

10.1038/sj.onc.1209096

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Prostate cancer remains a major cause of cancer-related mortality. Genetic clues to the molecular pathways driving the most aggressive forms of prostate cancer have been limited. Genetic inactivation of PTEN through either gene deletion or point mutation is reasonably common in metastatic prostate cancer and the resulting activation of phosphoinostide 3-kinase, AKT and mTOR provides a major therapeutic opportunity in this disease as mTOR inhibitors, HSP90 inhibitors and PI3K inhibitors begin to enter clinical development.

引用

收藏

页码：7465 / 7474

页数：10

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