ArticleNature2018
A metabolic function of FGFR3-TACC3 gene fusions in cancer.
Article in Nature, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
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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.
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Who cites it
130 citing papers in PubMed, 195 citations in OpenAlex.
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- 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
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Tumor DNA methylation subtypes predict immunotherapy outcomes in pleural mesothelioma patients in the NIBIT-EPI-MESO study.Nature genetics · 2026Article
- Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations.Cancer science · 2026Article
- Pharmacologic DPP-4 inhibition promotes CD8bioRxiv : the preprint server for biology · 2026Article
- A Unique Chimeric RNA: ERCC1-iASPP Drives Benzo[a]pyrene-Induced Lung Carcinogenesis via Dual Coding and Non-Coding Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- Glioblastoma resistance to EGFR antibody-drug conjugate is driven by transcriptional reprogramming and TEK-induced EGFR suppression.Journal of translational medicine · 2025Article
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- The Actin-Binding Prolyl-Isomerase Par17 Sustains Its Substrate Selectivity by Interdomain Allostery.Proteins · 2025Article
- Diffuse glioma withRadiology case reports · 2025Article
- Conundrum of 3N: nasopharyngeal nonkeratinizing non-viral carcinoma-reappraisal of fusions and report of two consecutive cases with unusual molecular findings.Virchows Archiv : an international journal of pathology · 2025Article
- Article
- Fibroblast growth factor receptor 3 mutation promotes HSPB6-mediated cuproptosis in hypochondroplasia by impairing chondrocyte autophagy.Journal of orthopaedic translation · 2025Article
- FGFR3::TACC3 fusions in head and neck carcinomas: a study of nine cases highlighting phenotypic heterogeneity, frequent HPV association, and a morphologically distinct subset in favor of a putative entity.Virchows Archiv : an international journal of pathology · 2025Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway.Frontiers in oncology · 2025Article
70 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 10 institutions in 5 countries.
Funding
Abstract
Chromosomal translocations that generate in-frame oncogenic gene fusions are notable examples of the success of targeted cancer therapies. We have previously described gene fusions of FGFR3-TACC3 (F3-T3) in 3% of human glioblastoma cases. Subsequent studies have reported similar frequencies of F3-T3 in many other cancers, indicating that F3-T3 is a commonly occuring fusion across all tumour types. F3-T3 fusions are potent oncogenes that confer sensitivity to FGFR inhibitors, but the downstream oncogenic signalling pathways remain unknown. Here we show that human tumours with F3-T3 fusions cluster within transcriptional subgroups that are characterized by the activation of mitochondrial functions. F3-T3 activates oxidative phosphorylation and mitochondrial biogenesis and induces sensitivity to inhibitors of oxidative metabolism. Phosphorylation of the phosphopeptide PIN4 is an intermediate step in the signalling pathway of the activation of mitochondrial metabolism. The F3-T3-PIN4 axis triggers the biogenesis of peroxisomes and the synthesis of new proteins. The anabolic response converges on the PGC1α coactivator through the production of intracellular reactive oxygen species, which enables mitochondrial respiration and tumour growth. These data illustrate the oncogenic circuit engaged by F3-T3 and show that F3-T3-positive tumours rely on mitochondrial respiration, highlighting this pathway as a therapeutic opportunity for the treatment of tumours with F3-T3 fusions. We also provide insights into the genetic alterations that initiate the chain of metabolic responses that drive mitochondrial metabolism in cancer.
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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.