MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR tyrosine kinase inhibitors.

摘要: We analyzed MET protein and copy number in NSCLC with or without EGFR mutations untreated tyrosine kinase inhibitors (TKIs). was examined 28 4 human bronchial epithelial cell lines (HBEC) 100 primary tumors using quantitative real-time PCR. Positive results were confirmed by array comparative genomic hybridization fluorescence in-situ hybridization. Total phospho-MET expression determined 24 2 HBEC Western blot. for exon 19 deletions, T790M, L858R. Knockdown of siRNA performed to examine the relation between activation. High-level amplification observed 3 lung that had not been treated EGFR-TKIs. highly expressed phosphorylated all high amplification. In contrast, 6 showed among 21 (p = 0.042). Furthermore, those harboring mutant 0.0039). siRNA-mediated knockdown abolished which gene amplified. By amplified down-regulated EGFR. Our indicated present mutation activated NSCLC.