MET

Also known as c-Met, MET exon 14 skipping

Tumour types

non-small cell lung cancer

MET encodes a receptor tyrosine kinase; oncogenic activation in NSCLC most often arises from splice-site alterations causing exon 14 skipping, rather than from point mutations in the kinase domain.

MET exon 14 skipping alterations are the primary actionable finding; MET amplification is a distinct, separately assessed mechanism of activation and of acquired resistance to EGFR TKIs.

Clinical significance

NSCLC with MET exon 14 skipping alterations is eligible for MET tyrosine kinase inhibitor therapy.
fda — FDA-approved product labeling for MET TKIs

FDA-approved treatments

Tabrecta (capmatinib) — Metastatic NSCLC with MET exon 14 skipping alterations, as detected by an FDA-approved test [fda]
Tepmetko (tepotinib) — Metastatic NSCLC with MET exon 14 skipping alterations [fda]

Prevalence

MET exon 14 skipping alterations occur in approximately 3%-4% of NSCLC, more common in older patients and those with sarcomatoid histology. [fda]

Tests / detection method

NGS (RNA-based assays preferred for splice variants)

Therapeutic pipeline

MET-directed antibody-drug conjugates (MET amplification) [fda]

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