Molecular analysis of lung adenocarcinomas that do not have mutations in the EGFR pathway and development of therapeutic strategies against them

EGFR酪氨酸激酶抑制剂对EGFR突变肺癌的疗效显著。然而，几乎所有的肿瘤都获得耐药性。对于很大一部分肺癌，有效的治疗靶点是未知的。在本研究中，我们证实HER2突变或MET扩增可能是治疗靶点，尽管它们的发生率很低。此外，我们发现EGFR基因T790M继发性突变与MET扩增在获得性耐药中存在反比关系。

EGFR tyrosine kinase inhibitor confers often dramatic response in lung cancer harboring EGFR mutation. However, virtually all the tumors acquire resistance. For large fraction of lung cancer, a efficacious therapeutic target is not known. In this study, we confirmed the HER2 mutation or MET amplification could be the therapeutic target although their incidences were low. Furthermore, we found a reciprocal relationship between T790M secondary mutation of the EGFR gene and MET amplification in acquire resistance.