ArticleHuman molecular genetics2013
Oncogenic FGFR3 gene fusions in bladder cancer.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 1 of them a synthesis that pooled it.
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Who cites it
218 citing papers in PubMed, 1 synthesis or guideline pooled it, 375 citations in OpenAlex.
- Association between the TACC3 rs798766 Polymorphism and Risk of Urinary Bladder Cancer: A Synthesis Based on Current Evidence.Disease markers · 2017Pooled it
- Detection, Characterization, and Inhibition of FGFR-TACC Fusions in IDH Wild-type Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015Trial
- Trial
- Multiomic profiling links L1 retrotransposition to genomic instability and ecDNA in bladder cancer.Nature communications · 2026Article
- Targeting fusion proteins in solid tumors: from oncogenic mechanisms to clinical interventions.Acta pharmacologica Sinica · 2026Review
- Multi-omic profiling defines three distinct molecular subtypes of urothelial carcinoma with implications for precision therapy.Clinical and translational medicine · 2026Article
- Review
- FGFs/FGFRs and neuroinflammatory diseases: mechanism, drug therapies and delivery systems.Journal of advanced research · 2025Review
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- Diffuse glioma withRadiology case reports · 2025Article
- Interferon-γ/Janus Kinase 1/STAT1 Signaling Represses Forkhead Box A1 and Drives a Basal Transcriptional State in Muscle-Invasive Bladder Cancer.The American journal of pathology · 2025Article
- Insulin receptor tyrosine kinase substrate in health and disease (Review).Molecular medicine reports · 2025Review
- Cell-free expression and SMA copolymer encapsulation of a functional receptor tyrosine kinase disease variant, FGFR3-TACC3.Scientific reports · 2025Article
- Transcriptome-wide association study identifies genes associated with bladder cancer risk.Scientific reports · 2025Article
- FGFR-Altered Urothelial Carcinoma: Resistance Mechanisms and Therapeutic Strategies.Targeted oncology · 2025Review
- Expert Consensus on the Diagnosis and Treatment of FGFR Gene-Altered Solid Tumors.Global medical genetics · 2024Review
- Epigenetic Biomarkers as a New Diagnostic Tool in Bladder Cancer-From Early Detection to Prognosis.Journal of clinical medicine · 2024Review
- FGFR3 alterations in bladder cancer: Sensitivity and resistance to targeted therapies.Cancer communications (London, England) · 2024Review
- Heterochromatin formation and remodeling by IRTKS condensates counteract cellular senescence.The EMBO journal · 2024Article
- The roles of FGFR3 and c-MYC in urothelial bladder cancer.Discover oncology · 2024Review
158 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
FGF receptor 3 (FGFR3) is activated by mutation or over-expression in many bladder cancers. Here, we identify an additional mechanism of activation via chromosomal re-arrangement to generate constitutively activated fusion genes. FGFR3-transforming acid coiled coil 3 (TACC3) fusions resulting from 4p16.3 re-arrangements and a t(4;7) that generates a FGFR3-BAI1-associated protein 2-like 1 (BAIAP2L1) fusion were identified in 4 of 43 bladder tumour cell lines and 2 of 32 selected tissue samples including the tumour from which one of the cell lines was derived. These are highly activated and transform NIH-3T3 cells. The FGFR3 component is identical in all cases and lacks the final exon that includes the phospholipase C gamma 1 (PLCγ1) binding site. Expression of the fusions in immortalized normal human urothelial cells (NHUC) induced activation of the mitogen-activated protein kinase pathway but not PLCγ1. A protein with loss of the terminal region alone was not as highly activated as the fusion proteins, indicating that the fusion partners are essential. The TACC3 fusions retain the TACC domain that mediates microtubule binding and the BAIAP2L1 fusion retains the IRSp53/MIM domain (IMD) that mediates actin binding and Rac interaction. As urothelial cell lines with FGFR3 fusions are extremely sensitive to FGFR-selective agents, the presence of a fusion gene may aid in selection of patients for FGFR-targeted therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.