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ERBB4 (HER4) Somatische Mutation / Verstärkung

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IDBIO-ERBB4
ArtBiomarker
Aliase
ERBB4 / HER4 MutationСоматична мутація / ампліфікація ERBB4 (HER4)
Statusreviewed 2026-05-04 | pending_clinical_signoff
ErkrankungenDIS-NSCLC
QuellenSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Biomarker-Fakten

Biomarker-Typgene_mutation
Angaben zur Mutation{"exon": "multiple; kinase domain (E872K, E317K) and extracellular domain; fusions (ERBB4-NRG1 pathway)", "functional_impact": "gain-of-function (ERBB4 homodimerization or heterodimerization with EGFR/HER2/HER3 → PI3K/AKT, MAPK)", "gene": "ERBB4", "variant_type": "activating missense; amplification; fusion (rare)"}
Messung
VerfahrenTumor-NGS-Panel (DNA); FISH für die Verstärkung; RNA-Seq für Fusionen
Nachschlagewerk für die Aktionsfähigkeit{"gene": "ERBB4", "variant": "activating_mutation"}
Verwandte BiomarkerBIO-EGFR BIO-ERBB2 BIO-ERBB3 BIO-NRG1

Anmerkungen

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.

Verwendet von

Therapeutische Relevanz