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ALK L1196M Gatekeeper Resistenzmutation

Deterministische Ansicht der Quelle YAML Entität. Klinische Autorität bleibt mit den zitierten Quell-IDs und Rezensenten Sign-off Zustand.

IDBIO-ALK-L1196M
ArtBiomarker
Aliase
ALK L1196M Gatekeeper-MutationALK L1196M — мутація резистентності (gatekeeper)ALK TorwartALK p.L1196M
Statusreviewed 2026-04-27 | pending_clinical_signoff
ErkrankungenDIS-IMT
QuellenSRC-ALEX-PETERS-2017 SRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Biomarker-Fakten

Biomarker-Typgene_mutation
Angaben zur Mutation{"exon": "23", "functional_impact": "gatekeeper resistance to crizotinib (1st-gen) and partial resistance to alectinib; sensitive to brigatinib, ceritinib, lorlatinib", "gene": "ALK", "hgvs_protein": "p.L1196M", "variant_type": "missense"}
Messung
VerfahrenctDNA NGS bei Progression; Tumorrebiopsie NGS
Einheitencategorical (positive | negative); VAF % when reported
Nachschlagewerk für die Aktionsfähigkeit‚Gen‘: ‚ALK‘, ‚Variante‘:‚L1196M‘}
Verwandte BiomarkerBIO-ALK-FUSION BIO-ALK-REARRANGEMENT BIO-ALK-G1202R

Anmerkungen

Classical ALK gatekeeper mutation (analogous to EGFR T790M, BCR::ABL1 T315I). Most frequently seen as acquired resistance after crizotinib (1st-gen). 2nd-generation TKIs (alectinib, brigatinib, ceritinib) retain activity — alectinib superiority over crizotinib in 1L (ALEX, Peters 2017) is partly explained by avoidance of L1196M-mediated resistance. Lorlatinib also active. Compound mutations involving L1196M (e.g., L1196M + G1202R) emerge under sequential TKI pressure and require trial-based strategies.

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Biomarker

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