ArticleActa neuropathologica communications2020
Genetic and epigenetic landscape of IDH-wildtype glioblastomas with FGFR3-TACC3 fusions.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 47 citations in OpenAlex.
- Pathway dysregulation and therapeutic resistance in glioblastoma: molecular mechanisms and emerging therapeutic targets.Future science OA · 2026Review
- Nationwide genomic data analysis of central nervous system tumors in Japan based on C-CAT database.International journal of clinical oncology · 2026Article
- Clinical and Genetic Landscape of Glioblastoma, IDH-Wildtype With FGFR Gene Family Alterations.Cancer science · 2026Article
- FGFR alterations and potential role of FGFR inhibitors in pediatric brain tumors.Neuro-oncology advances · 2026Review
- Detection of Copy-Number Variations in CNS Tumours From Off-Target Reads of Hybrid-Capture Sequencing.Neuropathology and applied neurobiology · 2026Article
- Diffusely metastatic glioblastoma with FGFR3::TACC3 fusion: cell-free DNA fragmentation analyses and molecular characterization of matched primary and metastatic tumor sites.Acta neuropathologica communications · 2025Article
- Diffuse glioma with FGFR3-TACC3 fusion in adults is not a homogenous clinicopathological and molecular entity.The journal of pathology. Clinical research · 2025Article
- Diffuse glioma withRadiology case reports · 2025Article
- Epigenetic Alterations in Glioblastoma Multiforme as Novel Therapeutic Targets: A Scoping Review.International journal of molecular sciences · 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
- Identification of the clinical and genetic characteristics of gliomas with gene fusions by integrated genomic and transcriptomic analysis.European journal of medical research · 2025Article
- A network-based discovery of prognostic markers in recurrent IDH wild-type gliomas.Frontiers in genetics · 2025Article
- Genomic medicine advances for brain tumors.International journal of clinical oncology · 2024Review
- Rare Oncogenic Fusions in Pediatric Central Nervous System Tumors: A Case Series and Literature Review.Cancers · 2024Review
- Diffuse Gliomas withCancers · 2024Review
- FGFR-targeted therapeutics: clinical activity, mechanisms of resistance and new directions.Nature reviews. Clinical oncology · 2024Review
- RT-PCR assay to detectNeuro-oncology practice · 2024Article
- The development of a custom RNA-sequencing panel for the identification of predictive and diagnostic biomarkers in glioma.Journal of neuro-oncology · 2024Article
- Clinicopathological and Molecular Characteristics ofBiomedicines · 2024Article
- Diffuse Gliomas with FGFR3-TACC3 Fusions: Oncogenic Mechanisms, Hallmarks, and Therapeutic Perspectives.Cancers · 2023Review
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 2 countries.
Funding
Abstract
A subset of glioblastomas (GBMs) harbors potentially druggable oncogenic FGFR3-TACC3 (F3T3) fusions. However, their associated molecular and clinical features are poorly understood. Here we analyze the frequency of F3T3-fusion positivity, its associated genetic and methylation profiles, and its impact on survival in 906 IDH-wildtype GBM patients. We establish an F3T3 prevalence of 4.1% and delineate its associations with cancer signaling pathway alterations. F3T3-positive GBMs had lower tumor mutational and copy-number alteration burdens than F3T3-wildtype GBMs. Although F3T3 fusions were predominantly mutually exclusive with other oncogenic RTK pathway alterations, they did rarely co-occur with EGFR amplification. They were less likely to harbor TP53 alterations. By methylation profiling, they were more likely to be assigned the mesenchymal or RTK II subclass. Despite being older at diagnosis and having similar frequencies of MGMT promoter hypermethylation, patients with F3T3-positive GBMs lived about 8 months longer than those with F3T3-wildtype tumors. While consistent with IDH-wildtype GBM, F3T3-positive GBMs exhibit distinct biological features, underscoring the importance of pursuing molecular studies prior to clinical trial enrollment and targeted treatment.
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Registered trials
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