ArticleNature communications2019
H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3 and is essential for glioma tumorigenesis.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 2 of them syntheses that pooled it.
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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
219 citing papers in PubMed, 2 syntheses or guidelines pooled it, 379 citations in OpenAlex.
- Biomarkers for prognosis of meningioma patients: A systematic review and meta-analysis.PloS one · 2024Pooled it
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- ONC201/dordaviprone for H3 K27M-mutant tumors: Discovery, mechanisms, therapeutic potential, and future directions.Genes & diseases · 2027Review
- Machine learning and computational approaches to model therapeutic response and resistance in diffuse midline glioma.Journal of neuro-oncology · 2026Review
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- Exon-skipping antisense oligonucleotides for H3.3K27M-altered diffuse midline glioma therapy.Molecular therapy. Nucleic acids · 2026Article
- Histone tail mutants: versatile tools for decoding chromatin, development, and disease.Trends in genetics : TIG · 2026Review
- Cell autonomous regional differences in oligodendrocyte lineage development and responses to oncohistone H3.3 K27M.Nature communications · 2026Article
- From chromatin dynamics to brain disease: Polycomb-Trithorax mechanisms in neurodevelopment.Trends in neurosciences · 2026Review
- ATRX inactivation disrupts global chromatin state and topology to dysregulate neurodevelopmental pathways in glioma pathogenesis.Nucleic acids research · 2026Article
- H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs.Nature genetics · 2026Article
- Efficacy of chemoradiotherapy in pediatric H3K27M-mutant diffuse intrinsic pontine glioma: a study based on single-center and SEER data.Journal of neuro-oncology · 2026Article
- Elongin B orchestrates chromatin and transcriptional programs in H3K27M-mutant diffuse midline glioma.bioRxiv : the preprint server for biology · 2026Article
- Evidence for coordinate CTCF and histone H3.3 activities in K27M diffuse midline gliomas.Acta neuropathologica communications · 2026Article
- A new hope: Clinical advances in targeted therapies for pediatric diffuse midline glioma.Neuro-oncology advances · 2026Review
- Dissecting polycomb complexes for enhanced fetal hemoglobin production.bioRxiv : the preprint server for biology · 2026Article
- RNA N6-methyladenosine (m6A) regulates cell cycle progression in diffuse midline glioma (DMG) and confers sensitivity to FTO inhibition.Cell death & disease · 2026Article
- De novo H3.3K27M-altered diffuse midline glioma in human brainstem organoids to dissect GD2 CAR T cell function.Nature cancer · 2026Article
- EZHIP in Pediatric Brain Tumors: From Epigenetic Mimicry to Therapeutic Vulnerabilities.International journal of molecular sciences · 2026Review
- Multiplexed measurements of protein-protein interactions and protein abundance across cellular conditions using Prod&PQ-seq.bioRxiv : the preprint server for biology · 2026Article
159 more citing papers are in PubMed but not listed here.
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33 authors at 12 institutions in 4 countries.
Funding
Abstract
Lys-27-Met mutations in histone 3 genes (H3K27M) characterize a subgroup of deadly gliomas and decrease genome-wide H3K27 trimethylation. Here we use primary H3K27M tumor lines and isogenic CRISPR-edited controls to assess H3K27M effects in vitro and in vivo. We find that whereas H3K27me3 and H3K27me2 are normally deposited by PRC2 across broad regions, their deposition is severely reduced in H3.3K27M cells. H3K27me3 is unable to spread from large unmethylated CpG islands, while H3K27me2 can be deposited outside these PRC2 high-affinity sites but to levels corresponding to H3K27me3 deposition in wild-type cells. Our findings indicate that PRC2 recruitment and propagation on chromatin are seemingly unaffected by K27M, which mostly impairs spread of the repressive marks it catalyzes, especially H3K27me3. Genome-wide loss of H3K27me3 and me2 deposition has limited transcriptomic consequences, preferentially affecting lowly-expressed genes regulating neurogenesis. Removal of H3K27M restores H3K27me2/me3 spread, impairs cell proliferation, and completely abolishes their capacity to form tumors in mice.
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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.