ArticleCell stem cell2021
Regional identity of human neural stem cells determines oncogenic responses to histone H3.3 mutants.
Article in Cell stem cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 80 citations in OpenAlex.
- Predicting recurrent glioblastoma clinical outcome to immune checkpoint inhibition and low-dose bevacizumab with tumor in situ fluid circulating tumor DNA analysis.Cancer immunology, immunotherapy : CII · 2024Trial
- Cell autonomous regional differences in oligodendrocyte lineage development and responses to oncohistone H3.3 K27M.Nature communications · 2026Article
- Forebrain Lineage Factor DMRTA2 Is Not Required for Maintenance of H3G34-Mutant Paediatric High-Grade Gliomas.Journal of cellular and molecular medicine · 2026Article
- Clinical Outcomes and Prognostic Features of Diffuse Hemispheric Glioma, H3 G34-Mutant: An International Multi-institutional Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Therapeutic efficacy of dendritic cell vaccination in a novel syngeneic mouse model of diffuse hemispheric glioma, H3 G34-mutant.Journal of neuro-oncology · 2026Article
- Pediatric H3 G34-mutant diffuse hemispheric glioma: clinical, imaging and molecular prognostic factors, MGMT expression, and temozolomide response.Acta neuropathologica · 2026Article
- DMRTA2 Regulates Radial Glial Maintenance and Tumorigenicity of Paediatric High-Grade Glioma.Journal of cellular and molecular medicine · 2026Article
- SOX2 phosphorylation during mitosis limits genomic damage.Genes & development · 2026Article
- De novo H3.3K27M-altered diffuse midline glioma in human brainstem organoids to dissect GD2 CAR T cell function.Nature cancer · 2026Article
- G34R cancer mutation alters the conformational ensemble and dynamics of the histone H3.3 tails.Nucleic acids research · 2026Article
- Modeling pediatric brain tumors with human stem cells.Frontiers in cellular neuroscience · 2026Review
- Olig1/2 Orchestrates Progenitor Cell Fates during Mammalian Cortical Gliogenesis and Gliomagenesis.Nature communications · 2025Article
- The Bermuda Triangle of paediatric brain cancers: epigenetics, developmental timing window and cell of origin.Cancer metastasis reviews · 2025Review
- Single-Cell Profiling of Pediatric High-Grade Gliomas Reveals OPC-Like Subpopulations Driving Tumorigenic Lineage Transitions.Pediatric discovery · 2025Article
- Zmynd11 is essential for neurogenesis by coordinating H3K36me3 modification of Epha2 and PI3K signaling pathway.Cell & bioscience · 2025Article
- FOXR2 Targets LHX6+/DLX+ Neural Lineages to Drive Central Nervous System Neuroblastoma.Cancer research · 2025Article
- The Role of Chronic Inflammation in Pediatric Cancer.Cancers · 2025Review
- Epigenetic modifications and their roles in pediatric brain tumor formation: emerging insights from chromatin dysregulation.Frontiers in oncology · 2025Review
- (B)On(e)-cohistones and the epigenetic alterations at the root of bone cancer.Cell death and differentiation · 2025Review
- Epigenetic reprogramming in pediatric gliomas: from molecular mechanisms to therapeutic implications.Trends in cancer · 2024Review
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17 authors at 4 institutions in 2 countries.
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Abstract
Point mutations within the histone H3.3 are frequent in aggressive childhood brain tumors known as pediatric high-grade gliomas (pHGGs). Intriguingly, distinct mutations arise in discrete anatomical regions: H3.3-G34R within the forebrain and H3.3-K27M preferentially within the hindbrain. The reasons for this contrasting etiology are unknown. By engineering human fetal neural stem cell cultures from distinct brain regions, we demonstrate here that cell-intrinsic regional identity provides differential responsiveness to each mutant that mirrors the origins of pHGGs. Focusing on H3.3-G34R, we find that the oncohistone supports proliferation of forebrain cells while inducing a cytostatic response in the hindbrain. Mechanistically, H3.3-G34R does not impose widespread transcriptional or epigenetic changes but instead impairs recruitment of ZMYND11, a transcriptional repressor of highly expressed genes. We therefore propose that H3.3-G34R promotes tumorigenesis by focally stabilizing the expression of key progenitor genes, thereby locking initiating forebrain cells into their pre-existing immature state.
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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.