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MET alterations (exon 14 skipping or amplification)

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDBIO-MET
TypeBiomarker
Aliases
MET alterationsMET amplificationMET ex14METex14Альтерації MET (пропуск екзону 14 або амплифікація)
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025 SRC-ONCOKB

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "Loss of CBL-mediated ubiquitination (ex14) or constitutive HGF-independent signaling (amplification)", "gene": "MET", "gene_hugo_id": "HGNC:7029", "hotspots": ["exon 14 skipping (MET ex14 / METex14, splice-site disruption around exon 14)", "MET amplification (high-level: GCN ≥10 or MET/CEP7 ≥4)"], "variant_type": "splice / amplification"}
Measurement
MethodTumor-tissue NGS (DNA + RNA panel preferred for ex14) OR ctDNA NGS OR FISH (amplification) OR IHC screening
Unitscategorical (ex14: positive/negative); copy number ratio (amplification)
Sensitivity requirementRNA-NGS preferred for ex14 to capture splice-site variants outside hotspots; FISH for amplification (MET/CEP7 ≥4 = high)
Related biomarkersBIO-EGFR-MUTATION

Notes

MET ex14 occurs in ~3–4% of NSCLC adenocarcinoma; enriched in older patients, sarcomatoid histology. Capmatinib (GEOMETRY mono-1) and tepotinib (VISION) are approved for ex14-positive advanced NSCLC. High-level MET amplification (GCN ≥10) drives a subset of HCC and papillary RCC and is an actionable resistance mechanism in EGFR-mutant NSCLC progressing on osimertinib (combine osimertinib + savolitinib in trials).

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