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ERBB4 (HER4) mutation somatique / amplification

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IDBIO-ERBB4
TypeBiomarqueur
Alias
ERBB4 / mutation HER4Соматична мутація / ампліфікація ERBB4 (HER4)
Étatreviewed 2026-05-04 | pending_clinical_signoff
MaladiesDIS-NSCLC
SourcesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Données biomarqueurs

Type de biomarqueurgene_mutation
Détails de la mutation{"exon": "multiple; domaine kinase (E872K, E317K) et domaine extracellulaire; fusions (voie ERBB4-NRG1)", "functional_impact":"gain de fonction (homodimérisation ERBBA4 ou hétérodimérization avec EGFR/HER2/HER3 → PI3K/AKT, MAPK)", "générique": «ERBB4», "variant_type": „activation du malentendu; amplification; fusion (rare)"}
Mesure
MéthodePanneaux NGS de tumeurs (ADN); FISH pour amplification; ARN-seq pour fusions
Recherche de la faisabilité{"gene": "ERBB4", "variant": "activating_mutation"}
Biomarqueurs connexesBIO-EGFR BIO-ERBB2 BIO-ERBB3 BIO-NRG1

Notes

ERBB4 (HER4) is the fourth member of the ERBB/HER receptor tyrosine kinase family. Somatic mutations occur in ~2–3% of NSCLC (mixed histologies). Afatinib (pan-HER inhibitor) and neratinib have preclinical/early clinical activity against ERBB4-mutant tumors, but no prospective Phase III trial has demonstrated benefit in ERBB4-selected patients. Afatinib is FDA-approved for EGFR-mutant NSCLC and ERBB2-mutant NSCLC (exon 20) — ERBB4 mutation alone does not qualify for these approvals. NRG1 fusions (NRG1 is the primary ERBB4 ligand) are a distinct actionable alteration that activates ERBB3/ERBB4 signaling; afatinib and zenocutuzumab (bispecific anti-HER2/HER3) have shown activity in NRG1-fusion lung cancer. ERBB4 mutation per se is not currently an approved companion diagnostic target.

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Pertinence thérapeutique