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KRAS Inhibitor Resistance in MET-Amplified KRAS G12C Non-Small Cell Lung Cancer Induced By RAS- and Non-RAS-Mediated Cell Signaling Mechanisms.

Shinichiro SuzukiKimio YonesakaTakeshi TeramuraToshiyuki TakeharaRyoji KatoHitomi SakaiKoji HarataniJunko TanizakiHiasto KawakamiHidetoshi HayashiKazuko SakaiKazuto NishioKazuhiko Nakagawa
Published in: Clinical cancer research : an official journal of the American Association for Cancer Research (2021)
MET amplification leads to the development of resistance to KRAS G12C inhibitors in NSCLC. Dual blockade of MET and KRAS G12C could be a treatment option for MET-amplified, KRAS G12C-mutated NSCLC.
Keyphrases
  • wild type
  • tyrosine kinase
  • small cell lung cancer
  • single cell
  • mesenchymal stem cells
  • combination therapy