作者: Hiromasa Yamamoto , Shinichi Toyooka , Tetsuya Mitsudomi
DOI: 10.1016/J.LUNGCAN.2008.06.021
关键词: Point mutation 、 Cancer 、 Tyrosine kinase 、 Cancer research 、 T790M 、 Mutation 、 Erlotinib 、 Epidermal growth factor receptor 、 Gefitinib 、 Biology 、 Oncology 、 Pulmonary and Respiratory Medicine
摘要: The discovery of mutations in the tyrosine kinase domain epidermal growth factor receptor (EGFR) gene non-small cell lung cancer (NSCLC) accelerated research molecular-targeted therapy by EGFR-tyrosine inhibitors (TKIs), such as gefitinib and erlotinib. About 90% EGFR are clustered exons 19 (deletion) 21 (point mutation at codon 858) patients with these have great response to EGFR-TKIs. However, tumors that initially respond EGFR-TKIs almost inevitably become resistant later T790M secondary MET amplification reported account for mechanism this acquired resistance. In review, we summarize recent findings about mutations, amplification, alterations other related genes sensitivity resistance We also discuss from our studies relationship between molecular aberrant methylation tumor suppressor (TSGs), which indicates they pathogenesis cancer. accumulated important data confer further insights on translational research, providing us new strategies treatment NSCLCs.