ArticleThe Journal of clinical investigation2013
The tumorigenic FGFR3-TACC3 gene fusion escapes miR-99a regulation in glioblastoma.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.
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Who cites it
146 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 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
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Integrated high-resolution copy number and histomolecular analysis of diffuse hemispheric glioma, H3 G34-mutant reveals universal TP53 abnormalities.Brain pathology (Zurich, Switzerland) · 2026Article
- RNA-based precision medicine in glioblastoma driven by oncogenic gene fusions.Molecular therapy. Oncology · 2026Review
- Targeting fusion proteins in solid tumors: from oncogenic mechanisms to clinical interventions.Acta pharmacologica Sinica · 2026Review
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations.Cancer science · 2026Article
- Low-grade neuroepithelial tumor with FGFR1::TACC1 fusion: a clinicopathologic analysis of seven cases.Journal of neuro-oncology · 2026Article
- Identification of natural FGFR3 inhibitor for glioma using integrated computational and microRNA regulatory analysis.Scientific reports · 2026Article
- Development of microRNA-Based Glioblastoma Biomarkers Using Blood Plasma Specimens.Diagnostics (Basel, Switzerland) · 2026Article
- A diverse landscape of FGFR alterations and co-mutations suggests potential therapeutic strategies in pediatric low-grade gliomas.Nature communications · 2025Article
- FGFR inhibitors promote the autophagic degradation of IFN-γ-induced PD-L1 and alleviate the PD-L1-mediated transcriptional suppression of FGFR3-TACC3 in non-muscle-invasive bladder cancer.Cell death & disease · 2025Article
- Diffuse glioma withRadiology case reports · 2025Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Review
- FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway.Frontiers in oncology · 2025Article
- Pharmacological and Biological Targeting of FGFR1 in Cancer.Current issues in molecular biology · 2024Review
- Diffuse Gliomas withCancers · 2024Review
- Mechanistic insights and the clinical prospects of targeted therapies for glioblastoma: a comprehensive review.Experimental hematology & oncology · 2024Review
86 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 6 institutions in 4 countries.
Funding
Abstract
Fusion genes are chromosomal aberrations that are found in many cancers and can be used as prognostic markers and drug targets in clinical practice. Fusions can lead to production of oncogenic fusion proteins or to enhanced expression of oncogenes. Several recent studies have reported that some fusion genes can escape microRNA regulation via 3'-untranslated region (3'-UTR) deletion. We performed whole transcriptome sequencing to identify fusion genes in glioma and discovered FGFR3-TACC3 fusions in 4 of 48 glioblastoma samples from patients both of mixed European and of Asian descent, but not in any of 43 low-grade glioma samples tested. The fusion, caused by tandem duplication on 4p16.3, led to the loss of the 3'-UTR of FGFR3, blocking gene regulation of miR-99a and enhancing expression of the fusion gene. The fusion gene was mutually exclusive with EGFR, PDGFR, or MET amplification. Using cultured glioblastoma cells and a mouse xenograft model, we found that fusion protein expression promoted cell proliferation and tumor progression, while WT FGFR3 protein was not tumorigenic, even under forced overexpression. These results demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and generates an oncogenic protein that promotes tumorigenesis in glioblastoma.
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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.