ArticleGenes & cancer2015
The BRAF kinase domain promotes the development of gliomas in vivo.
Article in Genes & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- O-mannosylation and furin processing are critical maturation events for the KIAA1549 protein implicated in pediatric pilocytic astrocytomas.The Journal of biological chemistry · 2026Article
- Combining Molecular Dynamics and Machine Learning to Predict Drug Resistance Causing Variants of BRAF in Colorectal Cancer.Molecules (Basel, Switzerland) · 2025Article
- The histone H3.3 K27M mutation suppresses Ser31phosphorylation and mitotic fidelity, which can directly drive gliomagenesis.Current biology : CB · 2025Article
- Establishment and characterization of patient-derived xenograft of a rare pediatric anaplastic pleomorphic xanthoastrocytoma (PXA) bearing a CDC42SE2-BRAF fusion.Scientific reports · 2023Article
- Targeted therapy for pediatric low-grade glioma.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Article
- Clinicopathologic features of kinase fusion-related thyroid carcinomas: an integrative analysis with molecular characterization.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- BRAF inhibition in melanoma is associated with the dysregulation of histone methylation and histone methyltransferases.Neoplasia (New York, N.Y.) · 2020Article
- Article
- Activated MEK cooperates with Cdkn2a and Pten loss to promote the development and maintenance of melanoma.Oncogene · 2017Article
- Engineering and Functional Characterization of Fusion Genes Identifies Novel Oncogenic Drivers of Cancer.Cancer research · 2017Article
- New Molecular Considerations for Glioma: IDH, ATRX, BRAF, TERT, H3 K27M.Current neurology and neuroscience reports · 2017Review
- Article
- Recurrent MET fusion genes represent a drug target in pediatric glioblastoma.Nature medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
In-frame BRAF fusions have been observed in over 80% of sporadic pilocytic astrocytomas. In each fusion, the N-terminal autoinhibitory domain of BRAF is lost, which results in constitutive activation via the retained C-terminal kinase domain (BRAF-KD). We set out to determine if the BRAF-KD is sufficient to induce gliomas alone or in combination with Ink4a/Arf loss. Syngeneic cell lines demonstrated the transforming ability of the BRAF-KD following Ink4a/Arf loss. In vivo, somatic cell gene transfer of the BRAF-KD did not cause tumors to develop; however, gliomas were detected in 21% of the mice following Ink4a/Arf loss. Interestingly, these mice demonstrated no obvious symptoms. Histologically the tumors were highly cellular and atypical, similar to BRAF(V600E) tumors reported previously, but with less invasive borders. They also lacked the necrosis and vascular proliferation seen in BRAFV600E-driven tumors. The BRAF-KD-expressing astrocytes showed elevated MAPK signaling, albeit at reduced levels compared to the BRAF(V600E) mutant. Pharmacologic inhibition of MEK and PI3K inhibited cell growth and induced apoptosis in astrocytes expressing BRAF-KD. Our findings demonstrate that the BRAF-KD can cooperate with Ink4a/Arf loss to drive the development of gliomas and suggest that glioma development is determined by the level of MAPK signaling.
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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.