Mutation BRAF non V600 (classe II / classe III)
Vue déterministe de l'entité source de la LJAM. L'autorité clinique demeure avec les ID de la source cités et l'état d'approbation de l ́examinateur.
| ID | BIO-BRAF-CLASS-II-III |
|---|---|
| Type | Biomarqueur |
| Alias | Classe II BRAFBRAF Classe IIIBRAF D594BRAF G466BRAF G469ABRAF G469VBRAF K601EBRAF L597BRAF N581BRAF non V600 (classe II/III)Мутація BRAF не-V600 (клас II / клас III) |
| État | reviewed 2026-04-29 | pending_clinical_signoff |
| Maladies | Aucune déclaration |
| Sources | SRC-CIVIC SRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-MELANOMA-2025 SRC-NCCN-NSCLC-2025 |
Données biomarqueurs
| Type de biomarqueur | gene_mutation |
|---|---|
| Détails de la mutation | {"functional_impact": "Class II — RAF dimer formation independent of upstream RAS activation; intermediate kinase activity; resistant to monomer-selective Type-I RAF inhibitors (vemurafenib / dabrafenib / encorafenib alone). Class III — kinase-dead or impaired; signal via heterodimerisation with wild-type CRAF; require upstream RTK / RAS activation to drive MAPK signalling.\n", "gene": "BRAF", "gene_hugo_id": "HGNC:1097", "hotspots": ["Class II (RAS-independent dimers, intermediate-to-high kina... |
| Mesure | MéthodePanneau ADN-NGS (préféré) OU NGS ctDNA. PCR à point chaud limité à V600 — manque non-V600. Unitéscatégorique; rapporter la variante + classe (II vs III) explicitement Exigence de sensibilitéNGS standard; cellulaire tumoral ≥20% recommandé |
| Biomarqueurs connexes | BIO-BRAF-V600E BIO-BRAF-V600K BIO-KRAS |
Notes
~5-10% of BRAF-mutant tumors overall (NSCLC, melanoma, CRC) are non-V600; proportion higher in lung adeno where Class II / Class III combined approach the V600 cohort. Distinct from V600 in BOTH biology and therapy. Class II (G469A, K601E, L597) — RAF dimer formation drives signalling; monomer-selective BRAF inhibitors fail; MEK inhibitor (trametinib / binimetinib) monotherapy may show partial activity; pan-RAF dimer inhibitors (e.g., naporafenib / belvarafenib / exarafenib, lifirafenib) in trial. Class III (D594, G466, N581) — kinase-impaired; require upstream RTK activity; treat per RTK driver if present (e.g., EGFR or KRAS-G12C co-mutation), else MEK inhibition limited rationale. CRC Class II / III almost always co-occur with RAS or other MAPK alteration — distinct from V600E CRC (which is targetable per BEACON). Practice gap: PCR-only V600 hot-spot testing misses non-V600 entirely; full BRAF-region NGS required to detect.
Utilisé par
No reverse references found in the YAML corpus.