ArticleOncotarget2018
Oncogenic driver FGFR3-TACC3 is dependent on membrane trafficking and ERK signaling.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
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.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Research on Targeted Therapy for Malignant Tumors of the Biliary Tract.OncoTargets and therapy · 2026Review
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 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
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- The oncogenic fusion protein EML4-NTRK3 requires three salt bridges for stability and biological activity.Heliyon · 2024Article
- RAPID resistance to BET inhibitors is mediated by FGFR1 in glioblastoma.Scientific reports · 2024Article
- Critical domains for NACC2-NTRK2 fusion protein activation.PloS one · 2024Article
- FGFR3 and FGFR4 overexpression in juvenile nasopharyngeal angiofibroma: impact of smoking history and implications for personalized management.Journal of applied genetics · 2023Article
- Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives.Cancers · 2023Review
- Incidental detection of FGFR3 fusion via liquid biopsy leading to earlier diagnosis of urothelial carcinoma.NPJ precision oncology · 2023Article
- Kinase regulation by liquid-liquid phase separation.Trends in cell biology · 2023Review
- Oncogenic driver FGFR3-TACC3 requires five coiled-coil heptads for activation and disulfide bond formation for stability.Oncotarget · 2023Article
- Polymorphous low-grade neuroepithelial tumor of the young with FGFR3-TACC3 fusion mimicking high-grade glioma: case report and series of high-grade correlates.Frontiers in oncology · 2023Article
- FGFR3-TACCs3 Fusions and Their Clinical Relevance in Human Glioblastoma.International journal of molecular sciences · 2022Review
- HSP90-CDC37 functions as a chaperone for the oncogenic FGFR3-TACC3 fusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Frequent FGFR1 hotspot alterations in driver-unknown low-grade glioma and mixed neuronal-glial tumors.Journal of cancer research and clinical oncology · 2022Article
- Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidatesfor targeted treatment.Nature communications · 2021Article
- Review
- FGFR3 overexpression is a useful detection tool for FGFR3 fusions and sequence variations in glioma.Neuro-oncology practice · 2021Article
- The Evolving Role of FGFR2 Inhibitors in Intrahepatic Cholangiocarcinoma: From Molecular Biology to Clinical Targeting.Cancer management and research · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fusion proteins resulting from chromosomal translocations have been identified as oncogenic drivers in many cancers, allowing them to serve as potential drug targets in clinical practice. The genes encoding FGFRs, Fibroblast Growth Factor Receptors, are commonly involved in such translocations, with the FGFR3-TACC3 fusion protein frequently identified in many cancers, including glioblastoma, cervical cancer, bladder cancer, nasopharyngeal carcinoma, and lung adenocarcinoma among others. FGFR3-TACC3 retains the entire extracellular domain and most of the kinase domain of FGFR3, with its C-terminal domain fused to TACC3. We examine here the effects of targeting FGFR3-TACC3 to different subcellular localizations by appending either a nuclear localization signal (NLS) or a myristylation signal, or by deletion of the normal signal sequence. We demonstrate that the oncogenic effects of FGFR3-TACC3 require either entrance to the secretory pathway or plasma membrane localization, leading to overactivation of canonical MAPK/ERK pathways. We also examined the effects of different translocation breakpoints in FGFR3-TACC3, comparing fusion at TACC3 exon 11 with fusion at exon 8. Transformation resulting from FGFR3-TACC3 was not affected by association with the canonical TACC3-interacting proteins Aurora-A, clathrin, and ch-TOG. We have shown that kinase inhibitors for MEK (Trametinib) and FGFR (BGJ398) are effective in blocking cell transformation and MAPK pathway upregulation. The development of personalized medicines will be essential in treating patients who harbor oncogenic drivers such as FGFR3-TACC3.
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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.