The genetics and biology of KRAS in lung cancer

被引：76

作者：

Westcott, Peter M. K. ^{[1
,3
]}

To, Minh D. ^{[2
,3
]}

机构：

[1] Univ Calif San Francisco, Dept Surg, Pharmaceut Sci & Pharmacogen Program, San Francisco, CA 94115 USA

[2] Univ Calif San Francisco, Dept Surg, Thorac Oncol Program, San Francisco, CA 94115 USA

[3] Univ Calif San Francisco, Helen Diller Comprehens Canc Ctr, San Francisco, CA 94115 USA

来源：

CHINESE JOURNAL OF CANCER | 2013年 / 32卷 / 02期

基金：

美国国家科学基金会;

关键词：

KRAS; RAS; oncogene; lung cancer; K-RAS GENE; SYNTHETIC LETHAL INTERACTION; ADJUVANT CHEMOTHERAPY; PROTEIN TRANSFERASE; SOMATIC MUTATIONS; MOUSE; EXPRESSION; ADENOCARCINOMA; SUSCEPTIBILITY; ACTIVATION;

D O I：

10.5732/cjc.012.10098

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Mutational activation of KRAS is a common oncogenic event in lung cancer and other epithelial cancer types. Efforts to develop therapies that counteract the oncogenic effects of mutant KRAS have been largely unsuccessful, and cancers driven by mutant KRAS remain among the most refractory to available treatments. Studies undertaken over the past decades have produced a wealth of information regarding the clinical relevance of KRAS mutations in lung cancer. Mutant Kras-driven mouse models of cancer, together with cellular and molecular studies, have provided a deeper appreciation for the complex functions of KRAS in tumorigenesis. However, a much more thorough understanding of these complexities is needed before clinically effective therapies targeting mutant KRAS-driven cancers can be achieved.

引用

页码：63 / 70

页数：8

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