ArticleThe American journal of surgical pathology2013
Epithelioid GBMs show a high percentage of BRAF V600E mutation.
Article in The American journal of surgical pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
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Who cites it
115 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022Guideline
- BRAF-amplified glioblastoma patients have a worse prognosis than those with BRAF mutation and are associated with amplification of MET, RHEB and CUL1.BMC neurology · 2026Article
- Genomic analysis of PLNTY-like tumor progression into epithelioid glioblastoma: a case report.Acta neuropathologica communications · 2026Article
- Programmed cell death evasion in BRAF V600E-driven primary CNS tumors and thyroid cancer brain metastases.Frontiers in neurology · 2026Review
- Biomarkers for predicting immunotherapy response and resistance in glioblastoma.Frontiers in immunology · 2026Review
- Clinical Outcome of Patients with Epithelioid Glioblastoma Harboring BRAFV600E Mutation; A Single Institution Experience.South Asian journal of cancer · 2025Article
- Rapid response to BRAF/MEK inhibitor therapy within 2 weeks for high-grade glioma with leptomeningeal metastasis: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- Article
- Management of asynchronous multifocal adult glioblastoma with loss of BRAFActa neuropathologica communications · 2025Article
- Clinicopathological, immunohistochemical and therapeutic approaches on survival in patients with epithelioid glioblastoma: Institutional experience in the management of 58 patients.Neurosurgical review · 2024Article
- Efficacy of BRAF/MEK-inhibitor therapy for epithelioid glioblastoma with a novel BRAFV600 mutation.Acta neuropathologica communications · 2024Article
- TRIM24 Cooperates with Ras Mutation to Drive Glioma Progression through snoRNA Recruitment of PHAX and DNA-PKcs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Novel Clinical Trials and Approaches in the Management of Glioblastoma.Current oncology reports · 2024Review
- Case report: complete long-lasting response to multimodal third line treatment with neurosurgical resection, carmustine wafer implantation and dabrafenib plus trametinib in aFrontiers in oncology · 2024Article
- A patient-derived xenograft mouse platform from epithelioid glioblastoma provides possible druggable screening and translational study.American journal of cancer research · 2024Article
- Advancements in targeted and immunotherapy strategies for glioma: toward precision treatment.Frontiers in immunology · 2024Review
- Establishment and characterization of patient-derived xenograft of a rare pediatric anaplastic pleomorphic xanthoastrocytoma (PXA) bearing a CDC42SE2-BRAF fusion.Scientific reports · 2023Article
- From Theory to Practice: Implementing the WHO 2021 Classification of Adult Diffuse Gliomas in Neuropathology Diagnosis.Brain sciences · 2023Review
- Bridging the age gap: a review of molecularly informed treatments for glioma in adolescents and young adults.Frontiers in oncology · 2023Review
- Recent advances in label-free optical, electrochemical, and electronic biosensors for glioma biomarkers.Biomicrofluidics · 2023Review
55 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors.
Funding
Abstract
BRAF V600E mutation has been identified in up to 2/3 of pleomorphic xanthoastrocytomas (PXAs), World Health Organization grade II, as well as in varying percentages of PXAs with anaplastic features (PXA-A), gangliogliomas, extracerebellar pilocytic astrocytomas, and, rarely, giant cell glioblastoma multiforme (GC-GBMs). GC-GBMs and epithelioid GBMs (E-GBMs) can be histologically challenging to distinguish from PXA-A. We undertook this study specifically to address whether these 2 tumor types also showed the mutation. We tested our originally reported cohort of 8 E-GBMs and 2 rhabdoid GBMs (R-GBM) as well as 5 new E-GBMs (1 pediatric, 4 adult) and 9 GC-GBMs (2 pediatric, 7 adult) (n=24) for BRAF V600E mutational status. Twenty-one of 24 had sufficient material for IDH-1 immunostaining, which is usually absent in PXAs, PXA-As, and primary GBMs but present in secondary GBMs. Patients ranged in age from 4 to 67 years. BRAF V600E mutation was identified in 7/13 of E-GBMs, including 3 of our original cases; patients with mutation were aged 10 to 50 years. None of the 9 GC-GBMs or 2 R-GBMs manifested this mutation, including pediatric patients. The sole secondary E-GBM was the single case manifesting positive IDH-1 immunoreactivity. A high percentage of E-GBMs manifest BRAF V600E mutation, paralleling PXAs. All R-GBMs and GC-GBMs were negative, although larger multi-institutional cohorts will have to be tested to extend this result. BRAF V600E mutational analyses should be performed on E-GBMs, particularly in all pediatric and young-aged adults, given the potential for BRAF inhibitor therapy in this subset of GBM patients.
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