Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis

被引：998

作者：

Cully, M

You, H

Levine, AJ

Mak, TW

机构：

[1] Canc Inst New Jersey, New Brunswick, NJ USA

[2] Inst Adv Study, Princeton, NJ 08540 USA

来源：

NATURE REVIEWS CANCER | 2006年 / 6卷 / 03期

关键词：

D O I：

10.1038/nrc1819

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?

引用

收藏

页码：184 / 192

页数：9

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