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FGFR2 alterations (fusion / amplification / mutation)

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDBIO-FGFR2
TypeBiomarker
Aliases
BICC1-FGFR2FGFR2 alterationsFGFR2 fusionFGFR2-AHCYL1Альтерації FGFR2 (фузія / амплифікація / мутація)
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-HCC-2025 SRC-ONCOKB

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "Constitutive FGFR2 kinase activity (fusion); receptor stabilization (mutations)", "gene": "FGFR2", "gene_hugo_id": "HGNC:3689", "hotspots": ["BICC1-FGFR2 fusion (intrahepatic cholangiocarcinoma — most common partner)", "FGFR2-AHCYL1 fusion", "FGFR2-CCDC6 fusion", "Amplification (gastric, breast)", "Activating mutations in extracellular Ig-domains (S252W, Y375C)"], "variant_type": "fusion / amplification / missense"}
Measurement
MethodRNA-NGS (preferred, captures fusion partners) OR DNA-NGS (CN + mutations + fusion-aware) OR FISH break-apart
Unitscategorical (fusion: positive/negative); copy number ratio
Sensitivity requirementRNA-NGS preferred for fusion; ctDNA acceptable when tissue limited
Related biomarkersBIO-FGFR1 BIO-FGFR3-MUTATION

Notes

FGFR2 fusion present in ~10–20% of intrahepatic cholangiocarcinoma — the canonical actionable alteration in this disease. Pemigatinib (FIGHT-202) and futibatinib (FOENIX-CCA2) FDA-approved for advanced cholangiocarcinoma harboring FGFR2 fusion or rearrangement after ≥1 prior systemic therapy. Resistance: gatekeeper (V564F) and molecular-brake mutations — futibatinib (covalent) retains activity against some pemigatinib-resistance variants. FGFR2 amplification also a niche signal in gastric and breast.

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