ArticleCancer biology & therapy2014
Recurrent FGFR3-TACC3 fusion gene in nasopharyngeal carcinoma.
Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 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
- FGF/FGFR Alteration Type as a Candidate Enrichment Biomarker for Gunagratinib in Recurrent or Metastatic Head and Neck Cancer: An Exploratory Analysis of Two Early-Phase Trials.Targeted oncology · 2026Trial
- Review
- Anchored random reverse primer sequencing for quantitative detection of novel gene fusions.Nature biomedical engineering · 2026Article
- Review
- Prevalence and biological impact of clinically relevant gene fusions in head and neck cancers.NPJ precision oncology · 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
- TACC3 enhances glycolysis in bladder cancer cells through inducing acetylation of c-Myc.Cell death & disease · 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
- FGFR3-TACC3 fusion gene promotes glioblastoma malignant progression through the activation of STAT3 signaling pathway.Frontiers in oncology · 2025Article
- FGFR1/2/3-rearranged carcinoma of the head and neck: expanded histological spectrum crossing path with high-risk HPV in the sinonasal tract.Histopathology · 2024Article
- Molecular Targeting of the Fibroblast Growth Factor Receptor Pathway across Various Cancers.International journal of molecular sciences · 2024Review
- Clinicopathological and Molecular Characteristics ofBiomedicines · 2024Article
- Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives.Cancers · 2023Review
- Targeting FGFRs by pemigatinib induces G1 phase cell cycle arrest, cellular stress and upregulation of tumor suppressor microRNAs.Journal of translational medicine · 2023Article
- Anti-angiogenic therapy for advanced primary pulmonary lymphoepithelioma-like carcinoma: a retrospective multicenter study.Journal of cancer research and clinical oncology · 2023Article
- Oncogenic driver FGFR3-TACC3 requires five coiled-coil heptads for activation and disulfide bond formation for stability.Oncotarget · 2023Article
- Nasopharyngeal Carcinoma Progression: Accumulating Genomic Instability and Persistent Epstein-Barr Virus Infection.Current oncology (Toronto, Ont.) · 2022Review
- FGFR3-TACCs3 Fusions and Their Clinical Relevance in Human Glioblastoma.International journal of molecular sciences · 2022Review
- The microdissected gene expression landscape of nasopharyngeal cancer reveals vulnerabilities in FGF and noncanonical NF-κB signaling.Science advances · 2022Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasopharyngeal carcinoma (NPC) is one of the most common head and neck malignancies and exhibits regional differences in incidence. Because many fusion genes have been discovered in different types of tumors over the past few years, we aimed to investigate the existence of a fusion gene in primary NPC patients using RNA-seq. In this study, for the first time, we found that fibroblast growth factor receptor 3-transforming acidic coiled-coil-containing protein 3 (FGFR3-TACC3) fusion transcripts are recurrently detected in NPC. The presence of this fusion gene was also detected in head and neck cancer, esophageal squamous cell carcinoma (ESCC), and lung cancer. Furthermore, we found certain new isoforms of the FGFR3-TACC3 fusion transcripts, such as a gene fusion between exon 18 of FGFR3 and exon 6 or exon 14 of TACC3 and agene fusion between exon 19 of FGFR3 and exon 11 of TACC3. In addition, we showed that the FGFR3-TACC3 fusion gene promotes cell proliferation, colony formation, and transforming ability in vitro, whereas the FGFR3-TACC3 K508M mutant or treatment with the FGFR inhibitor PD173074 abrogates these effects, suggesting that FGFR3-TACC3 most likely exerts its effects through activation of FGFR kinase activity. This activation likely leads to the development of NPC. Additionally, FGFR3-TACC3 could trigger activation of the ERK and Akt signaling pathways, whereas FGFR3-TACC3 K508M mutant could not, suggesting that these 2 signaling pathways might be involved in the function of FGFR3-TACC3. Taken together, our data demonstrated the oncogenic role of FGFR3-TACC3 in vitro, indicating that FGFR3-TACC3 may be useful as a diagnostic marker and therapeutic target in cancers.
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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.