{"entity":{"id":"fgfr1","kind":"target","name":"FGFR1","aka":[],"tldr":"A growth receptor amplified in squamous lung cancer and fused in a rare blood cancer. Pemigatinib is approved for the FGFR1-rearranged myeloid and lymphoid neoplasm, and pan-FGFR drugs block FGFR1 too, which is why they raise blood phosphate.","summary":"FGFR1 is amplified in a minority of squamous lung and breast cancers and rearranged, most often with ZMYM2 or BCR, in the myeloid or lymphoid neoplasm with eosinophilia and FGFR1 rearrangement, an aggressive disease that responds to pemigatinib, approved for it in 2022. The pan-FGFR inhibitors erdafitinib, pemigatinib and futibatinib all inhibit FGFR1, and because FGFR1 in the kidney controls phosphate excretion, hyperphosphataemia is their shared class effect and dose marker. FGFR1 amplification alone has proved a weak predictor of response to FGFR inhibitors in solid tumours.","asOf":"2026-09-04","wikipedia":"https://en.wikipedia.org/wiki/Fibroblast_growth_factor_receptor_1","links":[{"label":"UniProt P11362: FGFR1","url":"https://www.uniprot.org/uniprotkb/P11362/entry"}],"tags":[],"related":[],"cancers":["myeloproliferative-neoplasms","nsclc"],"sections":[],"technologies":[],"targets":[],"drugs":["pemigatinib","erdafitinib","futibatinib"],"companies":[],"institutions":[],"pathways":["fgfr-signalling"],"terms":["gene-amplification"],"trials":[],"people":[],"bottlenecks":[],"keyPapers":["paper-weiss-fgfr1-amplification-squamous-lung-sci-transl-med-2010"],"journals":[],"dependsOn":[],"notes":["Lung cancer: focally amplified in 17 to 22% of squamous tumours and 2.7% of adenocarcinomas, the first therapeutically tractable alteration found in squamous disease (Weiss 2010; cBioPortal). It is also the standard example of amplification not equalling dependence: amplified cell lines die under FGFR inhibition, and patients selected on copy number alone have responded poorly."],"symbol":"FGFR1","role":[],"sources":[],"specificity":"broadly-expressed","distribution":"few-types","specificityNote":"Broadly expressed or essential: HPA finds the RNA at low tissue specificity; the 3 medicines aimed at it (Pemigatinib, Erdafitinib, Futibatinib) act on the wild-type protein, so normal tissue is exposed and the therapeutic window comes from the tumour's faster division or its dependence on the protein. HPA FGFR1: RNA low tissue specificity; high antibody staining in 6 normal tissues; highest cancer staining head and neck cancer (2 of 4 high). Distribution: 2 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lung cancer (all types), Myeloid neoplasms); approvals of single-target medicines aimed at it also list Biliary tract cancer (all types), Bladder & urothelial cancer, not counted; Open Targets associates it with 11 specific cancer types at or above 0.5 (encephalocraniocutaneous lipomatosis, renal cell carcinoma, urothelial carcinoma, pilocytic astrocytoma, colorectal cancer, non-small cell lung carcinoma and more). (Rule 7 of scripts/fetch-target-specificity.ts.)","specificitySources":[{"label":"Human Protein Atlas FGFR1 tissue","url":"https://www.proteinatlas.org/ENSG00000077782-FGFR1/tissue","note":"RNA tissue and blood lineage specificity, normal tissue antibody staining (version 25.1, CC BY-SA 3.0)"},{"label":"Open Targets ENSG00000077782 associations","url":"https://platform.opentargets.org/target/ENSG00000077782/associations","note":"cancer associations at or above 0.5 (CC0)"}],"hgnc":"HGNC:3688","ensembl":"ENSG00000077782","uniprot":"P11362","entrez":"2260","firstDescribed":1988,"firstDescribedBasis":"sequence","firstDescribedNote":"Earliest sequence paper UniProt cites for the protein: Ruta et al, Oncogene, 1988, \"A novel protein tyrosine kinase gene whose expression is modulated during endothelial cell differentiation\".","firstDescribedSource":"https://www.uniprot.org/uniprotkb/P11362/entry","biology":"Receptor tyrosine kinase; gene amplification in squamous cancers and fusions in the 8p11 myeloproliferative syndrome; renal FGFR1 mediates the hyperphosphataemia of pan-FGFR inhibitors.","whereFound":["Myeloid or lymphoid neoplasm with FGFR1 rearrangement","Squamous non-small-cell lung cancer (amplification)","Hormone receptor-positive breast cancer (amplification)","Non-small-cell lung cancer: focal high-level amplification 17-22%"],"targetClass":"kinase","prevalence":[{"cancerId":"nsclc","pct":"about 20","measure":"FGFR1 amplification in squamous cell carcinoma of the lung","source":"https://doi.org/10.1126/scitranslmed.3001451","note":"Weiss and colleagues found focal FGFR1 amplification in about a fifth of squamous lung cancers and rarely in adenocarcinoma."},{"cancerId":"nsclc","pct":"17-22","measure":"Focal high-level amplification","source":"https://www.cbioportal.org/study/summary?id=lusc_tcga_pan_can_atlas_2018","note":"cBioPortal high-level amplification: 83 of 487, 17.0%, in lusc_tcga_pan_can_atlas_2018; 30 of 178, 16.9%, in lusc_tcga_pub; 102 of 1,144, 8.9%, in the combined nsclc_tcga_broad_2016; against 14 of 511, 2.7%, in lung adenocarcinoma. Amplification was found in a systematic copy-number search of 155 squamous cell lung cancers and confirmed by fluorescence in situ hybridisation in 22% of an independent squamous cohort (Weiss 2010)."}]},"route":"/targets/fgfr1/","neighbours":{"cancer":[{"id":"myeloproliferative-neoplasms","kind":"cancer","name":"Myeloproliferative neoplasms (PV, ET, myelofibrosis)","route":"/cancers/myeloproliferative-neoplasms/"},{"id":"nsclc","kind":"cancer","name":"Non-small-cell lung cancer","route":"/cancers/nsclc/"}],"drug":[{"id":"erdafitinib","kind":"drug","name":"Erdafitinib","route":"/drugs/erdafitinib/"},{"id":"futibatinib","kind":"drug","name":"Futibatinib","route":"/drugs/futibatinib/"},{"id":"pemigatinib","kind":"drug","name":"Pemigatinib","route":"/drugs/pemigatinib/"}],"pathway":[{"id":"fgfr-signalling","kind":"pathway","name":"FGF / FGFR signalling","route":"/pathways/fgfr-signalling/"}],"term":[{"id":"gene-amplification","kind":"term","name":"Gene amplification and copy-number change","route":"/terms/gene-amplification/"}],"paper":[{"id":"paper-bluemn-double-negative-prostate-fgf-mapk-cancer-cell-2017","kind":"paper","name":"Androgen receptor pathway-independent prostate cancer is sustained through FGF signalling","route":"/key-papers/paper-bluemn-double-negative-prostate-fgf-mapk-cancer-cell-2017/"},{"id":"paper-tcga-lung-squamous-nature-2012","kind":"paper","name":"Comprehensive genomic characterization of squamous cell lung cancers","route":"/key-papers/paper-tcga-lung-squamous-nature-2012/"},{"id":"paper-weiss-fgfr1-amplification-squamous-lung-sci-transl-med-2010","kind":"paper","name":"Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer","route":"/key-papers/paper-weiss-fgfr1-amplification-squamous-lung-sci-transl-med-2010/"}]}}