EGF receptor mutations in lung cancer: From humans to mice and maybe back to humans

被引:32
作者
Arteaga, Carlos L. [1 ]
机构
[1] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Comprehens Canc Ctr, Breast Canc Res Program,Dept Med, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Sch Med, Vanderbilt Ingram Comprehens Canc Ctr, Breast Canc Res Program,Dept Canc Biol, Nashville, TN 37232 USA
关键词
D O I
10.1016/j.ccr.2006.05.014
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Deletions in exon 19 and nucleotide substitutions in exon 21 are the most common mutations of the EGFR (ErbB1) in NSCLC. These mutations endow the receptor with constitutive kinase activity. Most tumors expressing these mutants respond well to EGFR tyrosine kinase inhibitors, suggesting that they are dependent on mutant EGFR signaling. Two groups developed transgenic mice in which expression of these mutants is temporally induced in mouse lung. Mice expressing EGFR mutants develop bronchioloalveolar cancer and lung adenocarcinoma, which are highly sensitive to EGFR inhibitors. These mouse models provide important opportunities for studying the biology of NSCLC and the refinement of anti-EGFR therapies.
引用
收藏
页码:421 / 423
页数:3
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