ArticleNature cancer2025
Evolving cell states and oncogenic drivers during the progression of IDH-mutant gliomas.
Article in Nature cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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.
The trial behind it
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
27 citing papers in PubMed.
- Fibroblast growth factor receptor inhibition for succinate dehydrogenase-deficient gastrointestinal stromal tumors: a phase 2 trial.Nature medicine · 2026Trial
- Genes, fuel, and fate in lung cancer.Biochemical Society transactions · 2026Review
- Spatial analysis reveals the evolving organization of IDH-mutant glioma.Cancer cell · 2026Article
- Vorasidenib improves response to subsequent chemoradiation in a genetically engineered mouse model of IDH-mutant glioma.Science translational medicine · 2026Article
- Advances in Immunotherapy for Intrahepatic Cholangiocarcinoma.International journal of molecular sciences · 2026Review
- Longitudinal changes in DNA methylation in IDH-mutant glioma fuel disease progression through altered cell state differentiation.Nature genetics · 2026Article
- IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.Nature communications · 2026Article
- DNA copy number patterns reveal prognostic markers and elucidate mechanisms of evolution in IDH-mutant astrocytoma.Neuro-oncology · 2026Article
- Notch Overexpression Potentiates Interferon Signaling in Glioma Cells.Current issues in molecular biology · 2026Article
- Meningioma microenvironment harbors a rich immune landscape that evolves with biological state.Neuro-oncology · 2026Article
- From Epigenetic Constraint to Evolutionary Escape: Cell-State Transitions and Selective Pressures During Malignant Transformation in Lower-Grade Gliomas.Biomedicines · 2026Review
- Tumor-intrinsic chromatin programs enforce immune evasion in glioblastoma.The Journal of clinical investigation · 2026Article
- Redefining the immune microenvironment of gliomas in the era of single-cell genomics.Neuro-oncology advances · 2026Review
- Review
- Long-term administration of the mutant IDH inhibitor DS-1001b suppresses the growth of IDH1-mutant glioma in vitro and in mouse xenograft models and alters epigenetic profiles.Acta neuropathologica · 2026Article
- From Classical to Emerging Biomarkers of Brain and Central Nervous System Tumors. An Evidence-Based Review with a Focus on Gliomas.Cellular and molecular neurobiology · 2026Review
- A cell death program-based tumor signature stratifies prognosis, immune landscape, and therapeutic response in glioma.Frontiers in oncology · 2026Article
- Immunotherapy and targeted therapy for high grade gliomas: current and future directions.Journal of neuro-oncology · 2025Review
- Epigenetic reprogramming as the nexus of cancer stemness and therapy resistance: implications for biomarker discovery.Discover oncology · 2025Review
- Perioperative IDH inhibition in treatment-naive IDH-mutant glioma: a pilot trial.Nature medicine · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Isocitrate dehydrogenase (IDH) mutants define a class of gliomas that are initially slow-growing but inevitably progress to fatal disease. To characterize their malignant cell hierarchy, we profiled chromatin accessibility and gene expression across single cells from low-grade and high-grade IDH-mutant gliomas and ascertained their developmental states through a comparison to normal brain cells. We provide evidence that these tumors are initially fueled by slow-cycling oligodendrocyte progenitor cell-like cells. During progression, a more proliferative neural progenitor cell-like population expands, potentially through partial reprogramming of 'permissive' chromatin in progenitors. This transition is accompanied by a switch from methylation-based drivers to genetic ones. In low-grade IDH-mutant tumors or organoids, DNA hypermethylation appears to suppress interferon (IFN) signaling, which is induced by IDH or DNA methyltransferase 1 inhibitors. High-grade tumors frequently lose this hypermethylation and instead acquire genetic alterations that disrupt IFN and other tumor-suppressive programs. Our findings explain how these slow-growing tumors may progress to lethal malignancies and have implications for therapies that target their epigenetic underpinnings.
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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.