SynthesisNeuro-oncology2022
Prevalence of BRAFV600 in glioma and use of BRAF Inhibitors in patients with BRAFV600 mutation-positive glioma: systematic review.
Synthesis in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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Who cites it
46 citing papers in PubMed, 60 citations in OpenAlex.
- Response Rate and Molecular Correlates to Encorafenib and Binimetinib in BRAF-V600E Mutant High-Grade Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Practical management of BRAF inhibitors in glioma: toxicity and resistance.CNS oncology · 2026Review
- Phase I Evaluation of Patients with Newly Diagnosed Glioblastoma Treated with Radiation, Nivolumab, and IDO1 Enzyme Inhibitor BMS-986205.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Dual targeting of interlocked PTK2B and MAPK signaling triggers synergistic ferroptosis via autophagic flux disruption in BRAFCell communication and signaling : CCS · 2026Article
- BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Molecular biomedicine · 2026Review
- Window of opportunity study measuring defactinib and avutometinib delivery in glioblastomas.Cancer chemotherapy and pharmacology · 2026Article
- Clinical potential of [European journal of nuclear medicine and molecular imaging · 2026Article
- BRAF mutation and tumor immune microenvironment in new era.American journal of cancer research · 2026Review
- Leptomeningeal Dissemination in TERT Promoter-mutant Anaplastic Pleomorphic Xanthoastrocytoma Responding to BRAF-MEK Inhibition: A Case Report.NMC case report journal · 2026Article
- The BRAF V600E/MEK/ERK/METTL3 positive feedback loop regulates autophagy and promotes stemness and invasiveness in glioblastoma via mJournal of experimental & clinical cancer research : CR · 2025Article
- Unpredictable Evolution of Pilocytic Astrocytoma in Adults: A Case Series and Diagnostic Challenges.The American journal of case reports · 2025Article
- Dabrafenib in pediatric patients withNeuro-oncology practice · 2025Article
- Clinical experience with tovorafenib in adults with treatment-refractory high- and low-grade gliomas.Neuro-oncology practice · 2025Article
- Point/counterpoint: Upfront BRAF inhibition for adult BRAF-mutant high-grade gliomas.Neuro-oncology · 2025Article
- Glioblastoma in adults: A Society for Neuro-Oncology (SNO) and European Society of Neuro-Oncology (EANO) consensus review on current management and future directions.Neuro-oncology · 2025Review
- The excitatory milieu in glioma: Mechanisms and therapeutic avenues.Neuro-oncology · 2025Review
- 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
- BRAF/MEK inhibition induces cell state transitions boosting immune checkpoint sensitivity in BRAFCell reports. Medicine · 2025Article
- Novel insights toward diagnosis and treatment of glioneuronal and neuronal tumors in young adults.CNS oncology · 2024Review
- Recent studies on protein kinase signaling inhibitors based on thiazoles: review to date.RSC advances · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDetailed prevalence estimates of BRAFV600 mutations and BRAF inhibitor (BRAFi) treatment responses in V600-mutant glioma will inform trial development.
methodsOur systematic review analyzed overall prevalence of BRAFV600 mutations in glioma and BRAFi treatment response.
resultsBased on 13 682 patients in 182 publications, the prevalence of BRAFV600 in epithelioid glioblastoma (eGBM) was 69% [95% CI: 45-89%]; pleomorphic xanthoastrocytoma (PXA): 56% [48-64%] anaplastic pleomorphic xanthoastrocytoma (aPXA): 38% [23-54%], ganglioglioma (GG): 40% [33-46%], and anaplastic ganglioglioma (aGG): 46% [18-76%]. Prevalence in astroblastoma was 24% [8-43%], desmoplastic infantile astrocytoma (DIA): 16% [0-57%], subependymal giant cell astrocytoma (SEGA): 8% [0-37%], dysembryoplastic neuroepithelial tumor (DNET): 3% [0-11%], diffuse astrocytoma (DA): 3% [0-9%], and pilocytic astrocytoma (PA): 3% [2-5%]. We reviewed 394 V600-mutant gliomas treated with BRAFi from 130 publications. One hundred and twenty-nine pediatric low-grade gliomas showed 4 (3.1%) complete response (CR); 53 (41.1%) partial response (PR); 64 (49.6%) stable disease (SD) and 8 (6.2%) progressive disease (PD). 25 pediatric high-grade gliomas showed CR; PR; SD; PD in 4 (16.0%); 10 (40.0%), 4 (16.0%); and 7 (28.0%) respectively. Thirty-nine adult low-grade gliomas showed CR; PR; SD; PD of 4 (10.3%); 17 (43.6%); 16 (41.0%) and 2 (5.1%) respectively. Ninety-seven adult high-grade gliomas showed CR; PR; SD; PD of 6 (6.2%); 31 (32.0%); 27 (27.8%); and 33 (34.0%) respectively.
conclusionsBRAFV600 prevalence is highest in eGBM, PXA, aPXA, GG, aGG, and lower in astroblastoma, DIA, SEGA, DNET, DA, and PA. Our data provide the rationale for adjuvant clinical trials of BRAFi in V600-mutant glioma.
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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.