ArticleCancer cell2019
Histone H3.3 K27M Accelerates Spontaneous Brainstem Glioma and Drives Restricted Changes in Bivalent Gene Expression.
Article in Cancer cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 2 of them syntheses that pooled it.
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.
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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
185 citing papers in PubMed, 2 syntheses or guidelines pooled it, 313 citations in OpenAlex.
- Prediction of H3 K27M-mutant in midline gliomas by magnetic resonance imaging: a systematic review and meta-analysis.Neuroradiology · 2022Pooled it
- Association BetweenCancer control : journal of the Moffitt Cancer CenterPooled it
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 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
- A pontine-specific niche supports de novo gliomagenesis.Cell reports · 2026Article
- Integrated Proteomic and Metabolomic Analyses of Cerebrospinal Fluid from Pediatric Patients with Diffuse Intrinsic Pontine Glioma.International journal of molecular sciences · 2026Article
- Immunotherapy for Diffuse Midline Glioma: From Preclinical Modeling to Clinical Translation.Cancers · 2026Review
- H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs.Nature genetics · 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
- H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibition.bioRxiv : the preprint server for biology · 2026Article
- Article
- Deciphering the tumor microenvironment and role of immunotherapy in diffuse midline glioma: A scoping review.Neuro-oncology · 2026Article
- Metabolic dependencies and neural progenitor dysregulation: driving forces in paediatric high-grade glioma development.Cancer metastasis reviews · 2026Review
- De novo H3.3K27M-altered diffuse midline glioma in human brainstem organoids to dissect GD2 CAR T cell function.Nature cancer · 2026Article
- Radiotherapy plus neoadjuvant and concomitant IL-13Rα2-directed immunotoxin therapy for diffuse intrinsic pontine glioma.Communications biology · 2026Article
- Modeling pediatric brain tumors with human stem cells.Frontiers in cellular neuroscience · 2026Review
- Investigation of a global mouse methylome atlas reveals subtype-specific copy number alterations in pediatric cancer models.Nature genetics · 2026Article
- Modeling diffuse midline glioma through triple-electrode in utero electroporation of the developing mouse pons.PloS one · 2026Article
125 more citing papers are in PubMed but not listed here.
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Authors and funding
26 authors at 1 institution in 1 country.
Funding
Abstract
Diffuse intrinsic pontine gliomas (DIPGs) are incurable childhood brainstem tumors with frequent histone H3 K27M mutations and recurrent alterations in PDGFRA and TP53. We generated genetically engineered inducible mice and showed that H3.3 K27M enhanced neural stem cell self-renewal while preserving regional identity. Neonatal induction of H3.3 K27M cooperated with activating platelet-derived growth factor receptor α (PDGFRα) mutant and Trp53 loss to accelerate development of diffuse brainstem gliomas that recapitulated human DIPG gene expression signatures and showed global changes in H3K27 posttranslational modifications, but relatively restricted gene expression changes. Genes upregulated in H3.3 K27M tumors were enriched for those associated with neural development where H3K27me3 loss released the poised state of apparently bivalent promoters, whereas downregulated genes were enriched for those encoding homeodomain transcription factors.
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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.