Loading
When lung cancer switches on the MET receptor to bypass a blocked EGFR pill.
MET amplification is a bypass form of resistance in EGFR-mutant non-small-cell lung cancer: the tumour switches on the MET receptor to keep signalling while EGFR is blocked by a pill. It occurs in a substantial minority of osimertinib-resistant tumours and is one of the escape routes targeted by amivantamab, which binds both EGFR and MET. That dual mechanism underpins the MARIPOSA combination of amivantamab and lazertinib, and the same biology motivates MET tyrosine kinase inhibitor add-on trials such as INSIGHT 2 and SAVANNAH and c-MET antibody-drug conjugates such as telisotuzumab vedotin. The term sits within acquired resistance and the receptor tyrosine kinase activation pathway, and is linked from the resistance bottleneck and the resistance-routes map.
In plain words · A receptor that is either mutated in some lung cancers or amplified as an escape route when other lung cancer drugs fail.
Showing the target this term concerns: MET.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
It made MET exon 14 a clinical entity rather than a sequencing curiosity, and identified the patients most likely to be missed: older people whose age would otherwise argue against broad sequencing.
It is the reference frequency table for resistance to first-generation EGFR inhibitors, and it made rebiopsy at progression standard rather than exceptional, because the mechanism decides the next treatment and cannot be guessed.
The case for re-biopsy at progression, for treating resistance as a diagnosis rather than an endpoint, and for the idea of a drug holiday. It is also the origin of resistance-directed sequencing: what you give next should depend on what the tumour became.
It defined bypass resistance as a category and set the treatment rule that follows from it: keep blocking the original target and add an inhibitor of the bypass, which is the logic of every EGFR plus MET combination since.
Shares Amivantamab + lazertinib (first-line EGFR NSCLC), Resistance routes: how a blocked pathway comes back, Drug resistance (primary and acquired), Receptor tyrosine kinase activation.
Shares GEOMETRY mono-1, MET exon 14 skipping mutation, MET amplification (gene copy number), MET exon 14 mutations in non-small-cell lung cancer are associated with advanced age and stage-dependent MET genomic amplification and c-Met overexpression.
Shares MET amplification (gene copy number), MET exon 14 mutations in non-small-cell lung cancer are associated with advanced age and stage-dependent MET genomic amplification and c-Met overexpression, Telisotuzumab vedotin, MET.
Shares Amivantamab + lazertinib (first-line EGFR NSCLC), Amivantamab, MET, Acquired resistance to every therapy.
Shares MET exon 14 skipping mutation, MET amplification (gene copy number), MET exon 14 mutations in non-small-cell lung cancer are associated with advanced age and stage-dependent MET genomic amplification and c-Met overexpression, MET exon 14 and MET-amplified non-small-cell lung cancer.
Shares Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors, Resistance routes: how a blocked pathway comes back, Drug resistance (primary and acquired), Receptor tyrosine kinase activation.
Shares MET exon 14 skipping mutation, MET exon 14 and MET-amplified non-small-cell lung cancer, MET, Receptor tyrosine kinase activation.
Shares MET exon 14 skipping mutation, MET amplification (gene copy number), MET exon 14 mutations in non-small-cell lung cancer are associated with advanced age and stage-dependent MET genomic amplification and c-Met overexpression, MET.