Targeting the MET-Signaling Pathway in Non-Small-Cell Lung Cancer: Evidence to Date.
MET amplification
MET exon 14
MET pathway
non-small–cell lung cancer
Journal
OncoTargets and therapy
ISSN: 1178-6930
Titre abrégé: Onco Targets Ther
Pays: New Zealand
ID NLM: 101514322
Informations de publication
Date de publication:
2020
2020
Historique:
received:
23
03
2020
accepted:
30
05
2020
entrez:
2
7
2020
pubmed:
2
7
2020
medline:
2
7
2020
Statut:
epublish
Résumé
The c-MET proto-oncogene (MET) plays an important role in lung oncogenesis, affecting cancer-cell survival, growth and invasiveness. The MET receptor in non-small-cell lung cancer (NSCLC) is a potential therapeutic target. The development of high-output next-generation sequencing techniques has enabled better identification of anomalies in the MET pathway, like the MET exon-14 (METex14) mutation. Moreover, analyses of epidermal growth factor-receptor (EGFR) and mechanisms of resistance to tyrosine-kinase inhibitors (TKIs) demonstrated the importance of MET amplification as an escape mechanism in patients with TKI-treated EGFR-mutated NSCLCs. This review summarizes the laboratory findings on MET and its anomalies, trial results on METex14 alterations and MET amplification in non-EGFR mutated NSCLCs, and acquired resistance to TKI in EGFR-mutated NSCLCs. The outcomes of the first trials with anti-MET agents on non-selected NSCLC patients or those selected for MET overexpression were disappointing. Two situations seem the most promising today for the use of anti-MET agents to treat these patients: tumors harboring METex14 and those EGFR-sensitive mutation mutated under TKI-EGFR with a MET-amplification mechanism of resistance or EGFR-resistance mutation.
Identifiants
pubmed: 32606781
doi: 10.2147/OTT.S219959
pii: 219959
pmc: PMC7306460
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
5691-5706Informations de copyright
© 2020 Bylicki et al.
Déclaration de conflit d'intérêts
Dr Olivier Bylicki reports personal fees from ROCHE, personal fees from MSD, personal fees from ASTRA-ZENECA, during the conduct of the study. Professor Christos Chouaid reports grants, personal fees from Roche, grants, personal fees from AZ, grants, personal fees from Amgen, grants, personal fees from BMS, grants, personal fees from MSD, grants, personal fees from Bayer, grants, personal fees from Janssen, grants, personal fees from Pierre Fabre, grants, personal fees from Mundi Pharma, grants, personal fees from Takeda, grants, personal fees from Pfizer, personnal feesfrom Novartis, outside the submitted work. The other authors report no other conflicts of interest in this work.
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