ArticleDiagnostic pathology2017
A novel GIT2-BRAF fusion in pilocytic astrocytoma.
Article in Diagnostic pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Diagnostic Pitfalls of Oligodendroglioma-like Morphology: Integrated Reappraisal of 23 Non-Oligodendroglial Central Nervous System Tumors.Diagnostics (Basel, Switzerland) · 2026Article
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- Small Molecule Inhibitors as Therapeutic Agents Targeting Oncogenic Fusion Proteins: Current Status and Clinical.Molecules (Basel, Switzerland) · 2023Review
- Treatment of Pediatric Low-Grade Gliomas.Current neurology and neuroscience reports · 2023Review
- Unlocking the power of precision medicine for pediatric low-grade gliomas: molecular characterization for targeted therapies with enhanced safety and efficacy.Frontiers in oncology · 2023Review
- Tumor-Type Agnostic, Targeted Therapies: BRAF Inhibitors Join the Group.Acta medica academica · 2022Review
- The oncogenic fusion landscape in pediatric CNS neoplasms.Acta neuropathologica · 2022Review
- Implications of BRAF V600E mutation in gliomas: Molecular considerations, prognostic value and treatment evolution.Frontiers in oncology · 2022Review
- Discovery of a rareCancer biology & therapy · 2021Article
- Targetable BRAF and RAF1 Alterations in Advanced Pediatric Cancers.The oncologist · 2021Article
- Retrospective analysis of combination carboplatin and vinblastine for pediatric low-grade glioma.Journal of neuro-oncology · 2020Article
- Pediatric low-grade glioma in the era of molecular diagnostics.Acta neuropathologica communications · 2020Review
- Pilocytic astrocytomas: BRAFV600E and BRAF fusion expression patterns in pediatric and adult age groups.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019Article
- Development and Clinical Validation of a Large Fusion Gene Panel for Pediatric Cancers.The Journal of molecular diagnostics : JMD · 2019Article
- Review
- Management of pediatric low-grade glioma.Current opinion in pediatrics · 2019Review
- Article
- Effectiveness Treatment of a BRAF-ZKSCAN5 Fusion Gene Melanoma Case with Dabrafenib/Trametinib.Case reports in oncologyArticle
Corrections and comments
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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
backgroundKIAA1549-BRAF fusion is the most common genetic event in pilocytic astrocytoma (PA), and leads to activation of the mitogen activated protein kinase (MAPK) signaling pathway. Fusions of BRAF with other partner genes, as well as other genetic alterations not involving BRAF but also leading to MAPK pathway activation have been described rarely. CASE PRESENTATION: We present a new fusion partner in the low-grade glioma of a 10-year-old male, who presented with headaches and recent episodes of seizures. Magnetic resonance imaging (MRI) demonstrated a right temporal lobe tumor. Histological and immunohistochemical evaluation, and a next generation sequencing assay (Oncopanel, Illumina, 500 genes) including breaKmer analysis for chromosomal rearrangements were performed. Histology was remarkable for a low-grade glioma composed of mildly atypical astrocytes with piloid processes, in a focally microcystic background. Mitoses were not seen; unequivocal Rosenthal fibers or eosinophilic granular bodies were absent. The tumor was positive for OLIG2 and GFAP and negative for BRAF V600E and IDH1 R132H mutant protein immunostains. Oncopanel showed low SOX2 (3q26.33) copy number gain, and no gains at 7q34. There were no significant single nucleotide variants. BreaKmer detected a GIT2-BRAF fusion with loss of BRAF exons 1-8. The integrated diagnosis was low-grade glioma with piloid features, most consistent with pilocytic astrocytoma, WHO grade I.
conclusionGIT2-BRAF fusion has not been reported in the literature in any tumor. Given that the BRAF sequence deleted is identical to that seen in other fusion events in PA, it most likely acts as tumor driver by activation of the MAPK pathway.
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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.