赫拉
神经母细胞瘤RAS病毒癌基因同源物
克拉斯
生物
突变
基因
遗传学
癌症研究
癌症
表型
作者
Siqi Li,Allan Balmain,Christopher M. Counter
出处
期刊:Nature Reviews Cancer
[Springer Nature]
日期:2018-11-12
卷期号:18 (12): 767-777
被引量:266
标识
DOI:10.1038/s41568-018-0076-6
摘要
The three RAS genes - HRAS, NRAS and KRAS - are collectively mutated in one-third of human cancers, where they act as prototypic oncogenes. Interestingly, there are rather distinct patterns to RAS mutations; the isoform mutated as well as the position and type of substitution vary between different cancers. As RAS genes are among the earliest, if not the first, genes mutated in a variety of cancers, understanding how these mutation patterns arise could inform on not only how cancer begins but also the factors influencing this event, which has implications for cancer prevention. To this end, we suggest that there is a narrow window or 'sweet spot' by which oncogenic RAS signalling can promote tumour initiation in normal cells. As a consequence, RAS mutation patterns in each normal cell are a product of the specific RAS isoform mutated, as well as the position of the mutation and type of substitution to achieve an ideal level of signalling.
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