Laboratory of Translational Cancer Medicine, Candiolo Cancer Institute IRCCS, and Department of Oncology, University of Torino School of Medicine, Candiolo, Torino, Italy.
Cancer Discov. 2016 Dec;6(12):1306-1308. doi: 10.1158/2159-8290.CD-16-1181.
Anecdotal reports have shown that concomitant inhibition of EGFR and MET can be clinically effective in patients with non-small cell lung cancer carrying EGFR mutations and MET amplification, but large phase III trials in genetically unselected individuals have failed to confirm the benefit of this combination therapy. A new study corroborates the evidence that lung cancer susceptibility to EGFR and MET blockade is sustained by genetically based activation of both targets and identifies a mutation in MET that confers acquired resistance to standard MET inhibitors hitting the active kinase, yet is vulnerable to other MET-directed compounds with a different binding mode. Cancer Discov; 6(12); 1306-8. ©2016 AACR.See related article by Bahcall and colleagues, p. 1334.
已有报道显示，针对携带 EGFR 突变和 MET 扩增的非小细胞肺癌患者，同时抑制 EGFR 和 MET 可获得临床疗效，但在未进行基因选择的患者中进行的大型 III 期临床试验未能证实这种联合治疗的获益。一项新研究证实了这样的证据，即肺癌对 EGFR 和 MET 阻断的敏感性是由这两个靶点的基因激活所维持的，并确定了 MET 中的一个突变，该突变导致对标准 MET 抑制剂（靶向激酶的活性形式）产生获得性耐药，但易受其他具有不同结合模式的靶向 MET 的化合物影响。Cancer Discov; 6(12); 1306-8. ©2016 AACR. 请参阅 Bahcall 及其同事的相关文章，第 1334 页。
