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Article

Targeting MET in EGFR-Mutated NSCLC.

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer - 1 Jul 2026

Saw Stephanie P L, Li Molly S C, Park Sehhoon, Hatano Hiroto, Uehara Yuji, Menis Jessica, Brandão Mariana, Hendriks Lizza E L, Remon Jordi

Abstract excerpt

MET alterations, mainly gene amplification and protein overexpression, represent a major mechanism of primary and acquired resistance to EGFR tyrosine kinase inhibitors in EGFR-mutated (EGFRm) NSCLC. Both de novo and acquired MET dysregulation can activate downstream oncogenic signaling, providing a strong rationale for dual inhibition of EGFR and MET. This review summarizes the data for targeting MET alterations...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 41935667
DOI: 10.1016/j.jtho.2026.103711

Genes

MET
EGFR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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