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ALK L1196M mutation de résistance du gardien de porte

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IDBIO-ALK-L1196M
TypeBiomarqueur
Alias
ALK L1196M mutation de gardien de porteALK L1196M — мутація резистентності (gatekeeper)Porteuse ALKALK p.L1196M
Étatreviewed 2026-04-27 | pending_clinical_signoff
MaladiesDIS-IMT
SourcesSRC-ALEX-PETERS-2017 SRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Données biomarqueurs

Type de biomarqueurgene_mutation
Détails de la 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"}
Mesure
MéthodectDNA NGS à la progression; tumeur ré-biopsie NG
Unitéscategorical (positive | negative); VAF % when reported
Recherche de la faisabilité{"générique": "ALK", "variante":"L1196M"}
Biomarqueurs connexesBIO-ALK-FUSION BIO-ALK-REARRANGEMENT BIO-ALK-G1202R

Notes

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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