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FGFR1 alterations (amplification / mutation / fusion)

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

IDBIO-FGFR1
TypeBiomarker
Aliases
8p11.23 amplificationFGFR1 alterationsFGFR1 amplificationАльтерації FGFR1 (амплифікація / мутація / фузія)
Statusreviewed 2026-04-27 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025 SRC-ONCOKB

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"functional_impact": "Increased FGFR1 dosage and constitutive signaling", "gene": "FGFR1", "gene_hugo_id": "HGNC:3688", "hotspots": ["8p11.23 amplification (squamous NSCLC, breast luminal, HNSCC subset)", "Fusion (rare; FGFR1-TACC1 in glioma)", "Activating missense (rare)"], "variant_type": "amplification / fusion / missense"}
Measurement
MethodFISH (FGFR1/CEN8) OR DNA-NGS for copy number OR RNA-NGS for fusion
UnitsFGFR1/CEN8 ratio (≥2.0 commonly used); GCN cutoff varies
Sensitivity requirementThreshold not standardized — FGFR1/CEN8 ≥2.0 or GCN ≥6 commonly used in trials
Related biomarkersBIO-FGFR2 BIO-FGFR3-MUTATION

Notes

~15–20% of squamous NSCLC, ~10% of HR+ breast, subset of HNSCC and small-cell lung carcinoma. Predictive value of amplification alone is modest — earlier trials of multikinase FGFR inhibitors had limited responses; selective inhibitors (erdafitinib, pemigatinib, futibatinib) are primarily indicated for FGFR2/3 alterations. FGFR1 remains a prognostic / investigational target. Hyperphosphatemia is the on-target adverse effect of FGFR inhibition class-wide.

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Actionability

Biomarker