EGFR-targeted therapies in lung cancer: predictors of response and toxicity

被引：57

作者：

Heist, Rebecca Suk ^{[1
]}

Christiani, David ^{[1
]}

机构：

[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA 02114 USA

来源：

PHARMACOGENOMICS | 2009年 / 10卷 / 01期

关键词：

cancer genetics; EGFR; lung cancer; predictive markers; GROWTH-FACTOR-RECEPTOR; TYROSINE KINASE INHIBITORS; PHASE-II TRIAL; PREVIOUSLY TREATED PATIENTS; CETUXIMAB PLUS IRINOTECAN; KRAS MUTATIONS; GEFITINIB SENSITIVITY; MOLECULAR PREDICTORS; DINUCLEOTIDE REPEAT; MONOCLONAL-ANTIBODY;

D O I：

10.2217/14622416.10.1.59

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The EGFR pathway has emerged as a key target in non-small-cell lung cancer. EGF receptor (EGFR) inhibition in non-small-cell lung cancer is achieved via small molecular tyrosine kinase inhibitors, such as erlotinib or gefitinib, or monoclonal antibodies such as cetuximab. A growing body of evidence is identifying potential molecular predictors of response and toxicity. This includes tumor-related molecular markers, such as EGFR mutation and copy number, as well as germline markers such as polymorphisms in EGFR or EGFR pathway-related genes. This review focuses on the current state of knowledge of predictors of response and toxicity to EGFR inhibitors in lung cancer.

引用

页码：59 / 68

页数：10

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