Management of Non-small Cell Lung Cancer Patients with MET Exon 14 Skipping Mutations

Curr Treat Options Oncol. 2020 Apr 18;21(4):33. doi: 10.1007/s11864-020-0723-5.


The MET exon 14 skipping mutation is found in approximately 3% of lung adenocarcinomas and slightly more than 2% of lung squamous cell carcinomas. In recent years, more and more evidence has shown that MET inhibitors have achieved good anti-tumor effect in patients with MET exon 14 skipping mutation, suggesting that MET exon 14 skipping mutation may be a new target for NSCLC patients. Patients with positive MET exon 14 skipping mutation are recommended to be administered MET inhibitors, and crizotinib is recommended by the NCCN guideline. Due to the presence of gene amplification, second site mutation, bypass activation, and pathological type transformation, one of the inevitable problems of targeted therapy is drug resistance. If type I MET inhibitors (crizotinib, capmatinib, tepotinib, savolitinib) drug resistance is developed, type II MET inhibitors (cabozantinib, glesatinib, merestinib) can be considered.

Keywords: Clinical trial; MET exon 14 skipping mutation; Non-small cell lung cancer; Targeted therapy; Tyrosine kinase inhibitor.

Publication types

  • Review

MeSH terms

  • Alternative Splicing*
  • Antineoplastic Combined Chemotherapy Protocols / adverse effects
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Biomarkers, Tumor
  • Carcinoma, Non-Small-Cell Lung / diagnosis
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / therapy*
  • Cell Line, Tumor
  • Clinical Trials as Topic
  • Disease Management
  • Disease Susceptibility
  • Drug Resistance, Neoplasm
  • Exons*
  • Humans
  • Lung Neoplasms / diagnosis
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / therapy*
  • Molecular Targeted Therapy / methods
  • Mutation*
  • Prognosis
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins c-met / antagonists & inhibitors
  • Proto-Oncogene Proteins c-met / genetics*
  • Proto-Oncogene Proteins c-met / metabolism
  • Treatment Outcome


  • Biomarkers, Tumor
  • Protein Kinase Inhibitors
  • MET protein, human
  • Proto-Oncogene Proteins c-met