ArticleNeuro-oncology2022
Heterogeneity and excitability of BRAFV600E-induced tumors is determined by Akt/mTOR-signaling state and Trp53-loss.
Article in Neuro-oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 26 citations in OpenAlex.
- Sox2 protein stability is enhanced by BRafV600E and Pten deletion in adult neural stem/progenitor cells.NPJ precision oncology · 2026Article
- Single-nucleus RNA sequencing: immature excitatory neurons and transformed glia build human BRAFBrain communications · 2025Article
- WONOEP appraisal: The role of glial cells in focal malformations associated with early onset epilepsies.Epilepsia · 2024Review
- From bedside to bench: New insights in epilepsy-associated tumors based on recent classification updates and animal models on brain tumor networks.Molecular oncology · 2024Review
- Analysis of 1386 epileptogenic brain lesions reveals association with DYRK1A and EGFR.Nature communications · 2024Article
- Patient-Centered Management of Brain Tumor-Related Epilepsy.Current neurology and neuroscience reports · 2024Review
- Polymorphous Low-Grade Neuroepithelial Tumor of the Young (PLNTY): Scoping Review of Case Reports and Case Series.Asian journal of neurosurgery · 2024Article
- Ganglioglioma with adverse clinical outcome and atypical histopathological features were defined by alterations in PTPN11/KRAS/NF1 and other RAS-/MAP-Kinase pathway genes.Acta neuropathologica · 2023Article
- The genomic landscape across 474 surgically accessible epileptogenic human brain lesions.Brain : a journal of neurology · 2023Article
- Molecular Heterogeneity in BRAF-Mutant Gliomas: Diagnostic, Prognostic, and Therapeutic Implications.Cancers · 2023Review
- Successes and challenges in modeling heterogeneous BRAFFrontiers in oncology · 2023Review
- GABAScientific reports · 2022Article
- Neuropathology and epilepsy surgery: 2022 update.Free neuropathology · 2022Article
- Neuronal precursor cell persistence in ganglioglioma is associated with extracellular matrix remodeling and immune cell infiltration.Neuro-oncology advancesArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDevelopmental brain tumors harboring BRAFV600E somatic mutation are diverse. Here, we describe molecular factors that determine BRAFV600E-induced tumor biology and function.
methodsIntraventricular in utero electroporation in combination with the piggyBac transposon system was utilized to generate developmental brain neoplasms, which were comprehensively analyzed with regard to growth using near-infrared in-vivo imaging, transcript signatures by RNA sequencing, and neuronal activity by multielectrode arrays.
resultsBRAF V600E expression in murine neural progenitors elicits benign neoplasms composed of enlarged dysmorphic neurons and neoplastic astroglia recapitulating ganglioglioma (GG) only in concert with active Akt/mTOR-signaling. Purely glial tumors resembling aspects of polymorphous low-grade neuroepithelial tumors of the young (PLNTYs) emerge from BRAFV600E alone. Additional somatic Trp53-loss is sufficient to generate anaplastic GGs (aGGs) with glioneuronal clonality. Functionally, only BRAFV600E/pAkt tumors intrinsically generate substantial neuronal activity and show enhanced relay to adjacent tissue conferring high epilepsy propensity. In contrast, PLNTY- and aGG models lack significant spike activity, which appears in line with the glial differentiation of the former and a dysfunctional tissue structure combined with reduced neuronal transcript signatures in the latter.
conclusionmTOR-signaling and Trp53-loss critically determine the biological diversity and electrical activity of BRAFV600E-induced tumors.
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