ArticleCell2023
Modeling epigenetic lesions that cause gliomas.
Article in Cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 64 citations in OpenAlex.
- Gliomas phenocopy an inborn error of metabolism to drive neuronal activity and tumor growth.Cell · 2026Article
- A transcriptional biosensor reveals mechanisms of α-ketoglutarate signaling to chromatin.Science (New York, N.Y.) · 2026Article
- Longitudinal changes in DNA methylation in IDH-mutant glioma fuel disease progression through altered cell state differentiation.Nature genetics · 2026Article
- Disruption of CTCF binding by germline non-coding variants inmedRxiv : the preprint server for health sciences · 2026Article
- Single-cell multi-omic integration analysis prioritizes druggable genes and reveals cell-type-specific causal effects in glioblastomagenesis.Journal of translational medicine · 2026Article
- Murine modeling of IDH-mutant 1p/19q-codeleted oligodendroglioma reveals genotype specific phenotypes.bioRxiv : the preprint server for biology · 2026Article
- Pde4 mediates MHCII expression in oligodendroglia.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Trimodal single-cell profiling of transcriptome, epigenome and 3D genome in complex tissues with scHiCAR.Nature biotechnology · 2026Article
- CSRP2 modulates PDGFRA/PI3K/AKT signaling via PRC1 components in glioma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Oligodendrocyte: Development, Plasticity, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Nested ecosystems theory for conceptualizing brain tumors.Disease models & mechanisms · 2026Review
- Do Glioma Cells Rewire Neural Circuits through Epigenetic Changes? DNA Methylation Analysis of Genes Involved in Neuron-Glioma Communication in the Human Frontal Cortex.Journal of molecular neuroscience : MN · 2025Article
- Epigenetic reprogramming as the nexus of cancer stemness and therapy resistance: implications for biomarker discovery.Discover oncology · 2025Review
- Aberrant coupling of glutamate and tyrosine kinase receptors enables neuronal control of brain-tumor growth.Neuron · 2025Article
- Droplet Hi-C enables scalable, single-cell profiling of chromatin architecture in heterogeneous tissues.Nature biotechnology · 2025Article
- Targeting PDGFRA-SHP2 signaling enhances radiotherapy in IDH1-mutant glioma.Neuro-oncology · 2025Article
- Single-Cell Profiling of Pediatric High-Grade Gliomas Reveals OPC-Like Subpopulations Driving Tumorigenic Lineage Transitions.Pediatric discovery · 2025Article
- Brain Tumors, AI and Psychiatry: Predicting Tumor-Associated Psychiatric Syndromes with Machine Learning and Biomarkers.International journal of molecular sciences · 2025Review
- Ezh2 Regulates Early Astrocyte Morphogenesis and Influences the Coverage of Astrocytic Endfeet on the Vasculature.Cell proliferation · 2025Article
- RASGEF1C methylation for the distinguishment and classification of benign and malignant thyroid tumors.Clinical epigenetics · 2025Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Epigenetic lesions that disrupt regulatory elements represent potential cancer drivers. However, we lack experimental models for validating their tumorigenic impact. Here, we model aberrations arising in isocitrate dehydrogenase-mutant gliomas, which exhibit DNA hypermethylation. We focus on a CTCF insulator near the PDGFRA oncogene that is recurrently disrupted by methylation in these tumors. We demonstrate that disruption of the syntenic insulator in mouse oligodendrocyte progenitor cells (OPCs) allows an OPC-specific enhancer to contact and induce Pdgfra, thereby increasing proliferation. We show that a second lesion, methylation-dependent silencing of the Cdkn2a tumor suppressor, cooperates with insulator loss in OPCs. Coordinate inactivation of the Pdgfra insulator and Cdkn2a drives gliomagenesis in vivo. Despite locus synteny, the insulator is CpG-rich only in humans, a feature that may confer human glioma risk but complicates mouse modeling. Our study demonstrates the capacity of recurrent epigenetic lesions to drive OPC proliferation in vitro and gliomagenesis in vivo.
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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.