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MET amplification means extra copies of the MET gene, either as a primary driver in a few lung cancers or as the escape route after EGFR inhibitors. No label yet selects on it; trials define it by FISH ratio or copy number.
MET amplification is scored by FISH as MET/CEP7 ratio (high-level at 5 or more in the Camidge classification, or 2 or more with mean copies of 10 or more) or by sequencing as gene copy number (GCN 10 or more is the common trial threshold). It occurs de novo in 1 to 4 percent of NSCLC and arises in 5 to 20 percent of EGFR-mutant cancers progressing on osimertinib, the setting of the MARIPOSA-2 and the SAVANNAH trial of osimertinib plus savolitinib (NCT03778229). No approval names MET amplification as the selection criterion; amivantamab is approved on EGFR status rather than MET, and capmatinib's label covers exon 14 skipping only.
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.
MET amplification on your report does not yet open an approved treatment on its own. If your lung cancer is EGFR-mutant and grew on osimertinib, it is the reason trials combine a MET inhibitor with the EGFR drug, and your team may discuss those trials or amivantamab, which is approved on EGFR status.
Written only from the label or guideline text cited on this page. Not medical advice; your own report and the reading your team gives it come first.
MET/CEP7 ratio by FISH (high-level 5 or more) or MET gene copy number by sequencing (trial thresholds of 6 or 10 copies); no label defines a threshold.
“MET amplification (bypass resistance)”
SAVANNAH trial (NCT03778229): MET overexpression and/or amplification defined by IHC 90 percent 3+ or FISH 10 or more copiesNo approval uses this readout as a threshold. It is defined by SAVANNAH: osimertinib plus savolitinib in MET-amplified or overexpressed EGFR-mutant NSCLC after osimertinib (ClinicalTrials.gov NCT03778229).
Matched on the name and aliases of the readout in the title, setting and summary of each trial; a match is a mention, not proof the readout was an entry criterion.
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 Gene amplification and copy-number change, FISH / ISH (in situ hybridisation) and the tags biomarker, no-approval.
Shares MET exon 14 skipping mutation, Tepotinib, Capmatinib, MET amplification (bypass resistance).
Shares FISH / ISH (in situ hybridisation) and the tags biomarker, no-approval.
Shares Non-small-cell lung cancer and the tags biomarker, no-approval.
Shares the tags biomarker, no-approval.
Shares the tags biomarker, no-approval.
Shares EGFR T790M, Amivantamab, Non-small-cell lung cancer and the tag biomarker.
Shares Gene amplification and copy-number change, FISH / ISH (in situ hybridisation) and the tag biomarker.