AKT and cancer - Is it all mTOR?

被引：130

作者：

Rosen, Neal

She, Qing-Bai

机构：

[1] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA

[2] Mem Sloan Kettering Canc Ctr, Program Mol Pharmacol & Chem, New York, NY 10021 USA

来源：

CANCER CELL | 2006年 / 10卷 / 04期

关键词：

D O I：

10.1016/j.ccr.2006.10.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

AKT, a key regulator of cell proliferation and survival, is commonly dysregulated in human cancers. Activated AKT kinase is oncogenic and required for tumorigenesis in PTEN-deficient animals. However, the importance of AKT in mediating transformation by other oncogenes and which of its targets are necessary for this process are poorly understood. In this issue of Cancer Cell, Skeen et al. show that AKT is required for transformation by mutant H-Ras and for experimental skin carcinogenesis. Moreover, the effects of AKT are mediated predominantly or solely via mTORC1. This suggests that AKT or mTOR inhibitors will be useful treatments for many cancers.

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收藏

页码：254 / 256

页数：3

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