AI Article Synopsis
- Concomitant inhibition of EGFR and MET may help non-small cell lung cancer patients with specific mutations, but larger trials haven't supported this combo's effectiveness in a broader patient group.
- A new study suggests that certain genetic factors contribute to the effectiveness of targeting both EGFR and MET.
- It also identifies a mutation in MET that causes resistance to traditional MET inhibitors but remains susceptible to alternative MET-targeting drugs.
Article Abstract
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.
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| http://dx.doi.org/10.1158/2159-8290.CD-16-1181 | DOI Listing |
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