FGFR1

Chr 8AD

fibroblast growth factor receptor 1

Also known as: BFGFR, CD331, CEK, ECCL, FGFBR, FGFR-1, FLG, FLT-2

The encoded fibroblast growth factor receptor 1 protein contains an extracellular domain that binds fibroblast growth factors and an intracellular tyrosine kinase domain that activates downstream signaling cascades controlling cell proliferation and differentiation during development. Autosomal dominant mutations cause multiple craniosynostosis syndromes including Pfeiffer syndrome, Jackson-Weiss syndrome, and osteoglophonic dysplasia, as well as Kallmann syndrome with hypogonadotropic hypogonadism and anosmia. The pathogenic mechanism involves gain-of-function mutations that lead to premature suture fusion in craniosynostosis or loss-of-function mutations affecting hypothalamic-pituitary-gonadal axis development in Kallmann syndrome.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismADLOEUF 0.217 OMIM phenotypes
Clinical SummaryFGFR1
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Gene-Disease Validity (ClinGen)
Pfeiffer syndrome type 1 · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

3 total gene-disease associations curated

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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Clinical Trials
6 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — FGFR1
Authoritative clinical overview · Recommended first read
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Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.21LOEUF
pLI 1.000
Z-score 5.48
OE 0.09 (0.040.21)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
2.49Z-score
OE missense 0.69 (0.630.75)
348 obs / 505.2 exp
Mild constraint

Moderately missense-constrained (top ~2.5%)

Observed / Expected Ratios
LoF OE0.09 (0.040.21)
00.351.4
Missense OE0.69 (0.630.75)
00.61.4
Synonymous OE1.12
01.21.6
LoF obs/exp: 4 / 42.5Missense obs/exp: 348 / 505.2Syn Z: -1.40
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveFGFR1-related osteoglophonic dysplasiaGOFAD
definitiveFGFR1-related Pfeiffer syndromeGOFAD
definitiveFGFR1-related Hartsfield syndromeDNAD
definitiveFGFR1-related hypogonadotropic hypogonadism with or without anosmiaLOFAD
definitiveFGFR1-related encephalocraniocutaneous lipomatosisGOFAD
DN
0.5771th %ile
GOF
0.6637th %ile
LOF
0.60top 25%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function, gain-of-function and dominant-negative). The Badonyi & Marsh model scores gain-of-function highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF1 literature citation · LOEUF 0.21
GOFprediction above median · 1 literature citation
DN1 literature citation

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Literature Evidence

DNA dominant negative FGFR1 mutation identified in a Kallmann syndrome patient.PMID:26089778
GOFTRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jawPMID:30385747
LOFHere, we report a Japanese female patient with CPHD and FGFR1 haploinsufficiency.PMID:23657145

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

FGFR1 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

Lymphoma, Non-HodgkinMultiple MyelomaAdvanced Solid Tumors

Canadian Profiling and Targeted Agent Utilization Trial (CAPTUR)

RECRUITING
NCT03297606Phase PHASE2Canadian Cancer Trials GroupStarted 2018-03-23
OlaparibDasatinibNivolumab plus Ipilimumab
Lung CancerTKI ResistanceEGFR Sensitive Mutation

A Single Center, Single Arm Clinical Study on the Treatment of Advanced Non-small Cell Lung Cancer With Positive EGFR Sensitive Mutations and Failed EGFR TKIs With the Combination of Enrotinib and Paclitaxel Monoclonal Antibody

NOT YET RECRUITING
NCT06048315Phase PHASE3Degan LuStarted 2023-09
AnlotinibPenpulimab
Advanced Malignant Solid NeoplasmAnn Arbor Stage III Non-Hodgkin LymphomaAnn Arbor Stage IV Non-Hodgkin Lymphoma

Targeted Therapy Directed by Genetic Testing in Treating Pediatric Patients With Relapsed or Refractory Advanced Solid Tumors, Non-Hodgkin Lymphomas, or Histiocytic Disorders (The Pediatric MATCH Screening Trial)

ACTIVE NOT RECRUITING
NCT03155620Phase PHASE2National Cancer Institute (NCI)Started 2017-07-31
Biopsy ProcedureBiospecimen CollectionBone Marrow Aspiration and Biopsy
Locally Advanced CholangiocarcinomaIntrahepatic CholangiocarcinomaSolid Tumor

Safety and Anti-Tumor Activity of TYRA-200 in Advanced Cholangiocarcinoma With Activating FGFR2 Gene Alterations

RECRUITING
NCT06160752Phase PHASE1Tyra Biosciences, IncStarted 2023-11-22
Phase 1 Part A - dose escalation TYRA-200 taken once daily by mouth in 28-day cyclesPhase 1 Part B - dose expansion TYRA-200 taken once daily by mouth in 28-day cycles
Lymphoma, Non-HodgkinMultiple MyelomaAdvanced Solid Tumors

TAPUR: Testing the Use of Food and Drug Administration (FDA) Approved Drugs That Target a Specific Abnormality in a Tumor Gene in People With Advanced Stage Cancer

RECRUITING
NCT02693535Phase PHASE2American Society of Clinical OncologyStarted 2016-03-14
PalbociclibSunitinibTemsirolimus
CraniosynostosesCrouzon SyndromeSaethre Chotzen Syndrome

ASO Treatment for Syndromic Craniosynostoses

NOT YET RECRUITING
NCT07535372Fondazione Policlinico Universitario Agostino Gemelli IRCCSStarted 2026-04-20
Design of patient specific ASO
Clinical Literature
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Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
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