New driver mutations in non-small-cell lung cancer

被引：1056

作者：

Pao, William ^{[1
]}

Girard, Nicolas ^{[2
]}

机构：

[1] Vanderbilt Ingram Canc Ctr, Dept Med, Nashville, TN 37232 USA

[2] Univ Lyon 1, Hosp Civils Lyon, Louis Pradel Hosp, Dept Resp Med, F-69365 Lyon, France

来源：

LANCET ONCOLOGY | 2011年 / 12卷 / 02期

关键词：

GROWTH-FACTOR-RECEPTOR; EML4-ALK FUSION GENE; HER2 KINASE DOMAIN; SOMATIC MUTATIONS; TYROSINE KINASE; PIK3CA GENE; SIGNALING PATHWAY; COPY NUMBER; BRAF GENE; MET;

D O I：

10.1016/S1470-2045(10)70087-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Treatment decisions for patients with lung cancer have historically been based on tumour histology. Some understanding of the molecular composition of tumours has led to the development of targeted agents, for which initial findings are promising. Clearer understanding of mutations in relevant genes and their effects on cancer cell proliferation and survival, is, therefore, of substantial interest. We review current knowledge about molecular subsets in non-small-cell lung cancer that have been identified as potentially having clinical relevance to targeted therapies. Since mutations in EGFR and KRAS have been extensively reviewed elsewhere, here, we discuss subsets defined by so-called driver mutations in ALK, HER2 (also known as ERBB2), BRAF, PIK3CA, AKT1, MAP2K1, and MET The adoption of treatment tailored according to the genetic make-up of individual tumours would involve a paradigm shift, but might lead to substantial therapeutic improvements.

引用

页码：175 / 180

页数：6

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