ArticleScience (New York, N.Y.)2012
Transforming fusions of FGFR and TACC genes in human glioblastoma.
Article in Science (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 480 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
480 citing papers in PubMed, 2 syntheses or guidelines pooled it, 772 citations in OpenAlex.
- Receptor tyrosine kinase targeted therapies in glioblastoma: a systematic review.Frontiers in medicine · 2026Pooled it
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Infigratinib in Patients with Recurrent Gliomas and FGFR Alterations: A Multicenter Phase II Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Phase II Study of AZD4547 in Patients With Tumors Harboring Aberrations in the FGFR Pathway: Results From the NCI-MATCH Trial (EAY131) Subprotocol W.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Trial
- TBCRC 032 IB/II Multicenter Study: Molecular Insights to AR Antagonist and PI3K Inhibitor Efficacy in Patients with ARClinical cancer research : an official journal of the American Association for Cancer Research · 2020Trial
- Pathway dysregulation and therapeutic resistance in glioblastoma: molecular mechanisms and emerging therapeutic targets.Future science OA · 2026Review
- Next-generation therapeutics for glioblastoma: Challenges and future directions.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Anchored random reverse primer sequencing for quantitative detection of novel gene fusions.Nature biomedical engineering · 2026Article
- Review
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Translational perspectives on immunotherapy targets, germline syndromes, and novel fusions.The oncologist · 2026Article
- Artificial intelligence-based diagnostic model for identifying PTPRZ1-MET fusion in a clinically defined secondary glioblastoma cohort.Molecular biomedicine · 2026Article
- Article
- Targeting Kinase Signaling in Glioblastoma: Structural Optimization, Blood-Brain Barrier Dynamics and Combinatorial Translational Strategies.International journal of molecular sciences · 2026Review
- A subset of high-grade sarcomas with myogenic differentiation are associated with recurrent FGFR fusions.The journal of pathology. Clinical research · 2026Article
- RNA-based precision medicine in glioblastoma driven by oncogenic gene fusions.Molecular therapy. Oncology · 2026Review
- Stattic enhances the anti-tumor activity of AZD4547 in LUSC by blocking STAT3/RRM2-mediated DNA repair and inducing ROS-driven mitochondrial dysfunction.Cell death & disease · 2026Article
- Advances in targeted therapies for pediatric tumors.Acta pharmacologica Sinica · 2026Article
- 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
420 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 7 institutions in 3 countries.
Funding
Abstract
The brain tumor glioblastoma multiforme (GBM) is among the most lethal forms of human cancer. Here, we report that a small subset of GBMs (3.1%; 3 of 97 tumors examined) harbors oncogenic chromosomal translocations that fuse in-frame the tyrosine kinase coding domains of fibroblast growth factor receptor (FGFR) genes (FGFR1 or FGFR3) to the transforming acidic coiled-coil (TACC) coding domains of TACC1 or TACC3, respectively. The FGFR-TACC fusion protein displays oncogenic activity when introduced into astrocytes or stereotactically transduced in the mouse brain. The fusion protein, which localizes to mitotic spindle poles, has constitutive kinase activity and induces mitotic and chromosomal segregation defects and triggers aneuploidy. Inhibition of FGFR kinase corrects the aneuploidy, and oral administration of an FGFR inhibitor prolongs survival of mice harboring intracranial FGFR3-TACC3-initiated glioma. FGFR-TACC fusions could potentially identify a subset of GBM patients who would benefit from targeted FGFR kinase inhibition.
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What OpenQuestion holds
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.