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Activation of KRAS Mediates Resistance to Targeted Therapy in MET Exon 14-mutant Non-small Cell Lung Cancer.

Ken SuzawaMichael D OffinDaniel LuChristopher KurzatkowskiMorana VojnicRoger S SmithJoshua K SabariHuichun TaiMarissa MattarInna KhodosElisa de StanchinaCharles M RudinMark G KrisMaria E ArcilaWilliam W LockwoodAlexander DrilonMarc LadanyiRomel Somwar
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2018)
KRAS mutation is a recurrent mechanism of primary and secondary resistance to MET TKIs in METex14 lung cancers. Dual inhibition of MET or EGFR/ERBB2 and MEK may represent a potential therapeutic approach in this molecular cohort.
Keyphrases
  • tyrosine kinase
  • wild type
  • epidermal growth factor receptor
  • small cell lung cancer
  • cell proliferation