Sequencing analysis of BRAF mutations in human cancers

被引：13

作者：

Wooster, Richard ^{[1
]}

Futreal, Andrew P. ^{[1
]}

Stratton, Michael R. ^{[1
]}

机构：

[1] Wellcome Trust Sanger Inst, Canc Genome Project, Cambridge, MA USA

来源：

REGULATORS AND EFFECTORS OF SMALL GTPASES: RAS FAMILY | 2006年 / 407卷

关键词：

D O I：

10.1016/S0076-6879(05)07018-7

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

Cancers arise because of the accumulation of mutations in critical genes that alter normal programs of cell proliferation, differentiation, and death. The RAS-RAF-MEK-ERK-MAP kinase pathway mediates cellular responses to growth signals. RAS is mutated to an oncogenic form in approximately 15% of human cancer. The three RAF genes code for cytoplasmic serine/threonine kinases that are regulated by binding RAS. ARAF and c-RAF are infrequently mutated in human cancer. However, BRAF is mutated in a wide range of human cancers. Most mutations are within the kinase domain, with a single amino acid substitution (V600E) accounting for most mutations.

引用

页码：218 / +

页数：8

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