ArticleActa neuropathologica2015
Histone H3F3A and HIST1H3B K27M mutations define two subgroups of diffuse intrinsic pontine gliomas with different prognosis and phenotypes.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 359 papers, 4 of them syntheses that pooled it.
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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
359 citing papers in PubMed, 4 syntheses or guidelines pooled it, 655 citations in OpenAlex.
- Diffuse Midline H3K27-Altered Gliomas in the Spinal Cord: A Systematic Review.Journal of neuro-oncology · 2024Pooled it
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- Molecular Biomarker Testing for the Diagnosis of Diffuse Gliomas.Archives of pathology & laboratory medicine · 2022Guideline
- Prognostic Implication of Patient Age in H3K27M-Mutant Midline Gliomas.Frontiers in oncology · 2022Pooled it
- Targeted therapies plus radiotherapy for diffuse intrinsic pontine glioma: the randomized phase 2 BIOMEDE trial.Nature medicine · 2026Trial
- Phase 2 trial of veliparib, local irradiation, and temozolomide in patients with newly diagnosed high-grade glioma: a Children's Oncology Group study.Neuro-oncology · 2025Trial
- ACTION: a randomized phase 3 study of ONC201 (dordaviprone) in patients with newly diagnosed H3 K27M-mutant diffuse glioma.Neuro-oncology · 2024Trial
- Automated Determination of the H3 K27-Altered Status in Spinal Cord Diffuse Midline Glioma by Radiomics Based on T2-Weighted MR Images.AJNR. American journal of neuroradiology · 2023Trial
- Clinical outcomes of stereotactic biopsy on children with pontine diffuse midline glioma.Journal of neuro-oncology · 2023Trial
- Phase I/II trial of vorinostat and radiation and maintenance vorinostat in children with diffuse intrinsic pontine glioma: A Children's Oncology Group report.Neuro-oncology · 2022Trial
- 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 H3K27M variants determine myeloid subset dependencies and immune reprogramming in diffuse midline glioma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- From chromatin dynamics to brain disease: Polycomb-Trithorax mechanisms in neurodevelopment.Trends in neurosciences · 2026Review
- Clarification of the published survival analysis in H3F3B p.K27I-mutant diffuse midline glioma.Acta neuropathologica communications · 2026Article
- Harnessing the power of biomarkers for diffuse intrinsic pontine gliomas.Nature medicine · 2026Article
- Co-occurrence of pediatric-type diffuse high-grade gliomas with arteriovenous malformations: case report and narrative literature review.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026Review
- Evidence for coordinate CTCF and histone H3.3 activities in K27M diffuse midline gliomas.Acta neuropathologica communications · 2026Article
- Limited reliability of H3K27M detection using a commercially available blood-based comprehensive genomic profiling test in patients with diffuse midline gliomas: analysis of the nationwide C-CAT database in Japan.International journal of clinical oncology · 2026Article
- Concurrent chemoradiotherapy with temozolomide in newly pediatric diffuse intrinsic pontine glioma: clinical outcomes and safety analysis.Translational pediatrics · 2026Article
299 more citing papers are in PubMed but not listed here.
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19 authors at 9 institutions in 2 countries.
Funding
Abstract
Diffuse intrinsic pontine glioma (DIPG) is the most severe paediatric solid tumour, with no significant therapeutic progress made in the past 50 years. Recent studies suggest that diffuse midline glioma, H3-K27M mutant, may comprise more than one biological entity. The aim of the study was to determine the clinical and biological variables that most impact their prognosis. Ninety-one patients with classically defined DIPG underwent a systematic stereotactic biopsy and were included in this observational retrospective study. Histone H3 genes mutations were assessed by immunochemistry and direct sequencing, whilst global gene expression profiling and chromosomal imbalances were determined by microarrays. A full description of the MRI findings at diagnosis and at relapse was integrated with the molecular profiling data and clinical outcome. All DIPG but one were found to harbour either a somatic H3-K27M mutation and/or loss of H3K27 trimethylation. We also discovered a novel K27M mutation in HIST2H3C, and a lysine-to-isoleucine substitution (K27I) in H3F3A, also creating a loss of trimethylation. Patients with tumours harbouring a K27M mutation in H3.3 (H3F3A) did not respond clinically to radiotherapy as well, relapsed significantly earlier and exhibited more metastatic recurrences than those in H3.1 (HIST1H3B/C). H3.3-K27M-mutated DIPG have a proneural/oligodendroglial phenotype and a pro-metastatic gene expression signature with PDGFRA activation, while H3.1-K27M-mutated tumours exhibit a mesenchymal/astrocytic phenotype and a pro-angiogenic/hypoxic signature supported by expression profiling and radiological findings. H3K27 alterations appear as the founding event in DIPG and the mutations in the two main histone H3 variants drive two distinct oncogenic programmes with potential specific therapeutic targets.
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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.