Non-redundancy within the RAS oncogene family: Insights into mutational disparities in cancer

被引：37

作者：

Lau, Ken S.

Haigis, Kevin M. ^{[1
]}

机构：

[1] Massachusetts Gen Hosp, Mol Pathol Unit, Boston, MA 02114 USA

来源：

MOLECULES AND CELLS | 2009年 / 28卷 / 04期

关键词：

cancer; mutation; RAS; signaling; BLADDER-CARCINOMA ONCOGENE; K-RAS; N-RAS; TRANSFORMING GENES; PHOSPHOINOSITIDE; 3-KINASE; HUMAN-MELANOMA; HA-RAS; COLORECTAL-CANCER; SARCOMA-VIRUSES; SCID MICE;

D O I：

10.1007/s10059-009-0143-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The RAS family of oncoproteins has been studied extensively for almost three decades. While we know that activation of RAS represents a key feature of malignant transformation for many cancers, we are only now beginning to understand the complex underpinnings of RAS biology. Here, we will discuss emerging cancer genome sequencing data in the context of what is currently known about RAS function. Taken together, retrospective studies of primary human tissues and prospective studies of experimental models support the notion that the variable mutation frequencies exhibited by the RAS oncogenes reflect unique functions of the RAS oncoproteins.

引用

收藏

页码：315 / 320

页数：6

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