ReviewNeuro-oncology2024
H3K27M mutant glioma: Disease definition and biological underpinnings.
Review in Neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Machine learning radiomics for H3K27M mutation prediction in gliomas: A systematic review and meta-analysis.Neuroradiology · 2025Pooled it
- Outcomes of Laser Interstitial Thermal Therapy-Augmented Surgery in the Management of Subcortical Glioblastoma.Neurosurgery practice · 2026Article
- The DIPG/DMG National Tumor Board: The power of advocacy.Neuro-oncology pediatrics · 2026Article
- Selective histone deacetylase inhibition as a therapeutically relevant strategy in H3K27M-glioma.Neuro-oncology · 2026Article
- Histone tail mutants: versatile tools for decoding chromatin, development, and disease.Trends in genetics : TIG · 2026Review
- Modeling gliomas with organoids: Classification, fidelity, and guidelines for translational neuro-oncology.Neuro-oncology · 2026Review
- Single-cell multi-omic analyses resolve the cellular diversity of ALK/ROS1/MET/NTRK-fused gliomas in infants and older children.bioRxiv : the preprint server for biology · 2026Article
- Report of treatment intensity and survival outcomes in older patients with glioblastoma diagnosed according to WHO CNS 5 classification.Journal of neuro-oncology · 2026Observational
- Precision diagnosis and therapy for pediatric central nervous system tumors: consensus from the Brazilian Society of Pediatric Oncology (SOBOPE).Lancet regional health. Americas · 2026Review
- Comparative analysis of clinical characteristics and prognostic factors in adult and pediatric patients with H3K27M-mutant diffuse midline glioma.Neurosurgical review · 2026Article
- Epigenetic mechanisms and therapeutic advances in diffuse midline glioma (Review).Oncology reports · 2026Review
- Lactylation fuels nucleotide biosynthesis and facilitates deuterium metabolic imaging of tumor proliferation in preclinical models of H3K27M-mutant gliomas.Science translational medicine · 2026Article
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- A bibliometric analysis of progress and trends in pediatric glioma research.Discover oncology · 2026Article
- Differences in regional developmental origins of glioblastomas revealed by integrated molecular profiling.Journal of neuro-oncology · 2026Article
- Radiotherapy plus neoadjuvant and concomitant IL-13Rα2-directed immunotoxin therapy for diffuse intrinsic pontine glioma.Communications biology · 2026Article
- Cancer histone H2A.Z missense mutations disrupt function through distinct local and allosteric effects.Research square · 2026Article
- Article
- AI-augmented intraoperative decision-making workflows in diffuse midline glioma biopsy using cryosection pathology.Nature communications · 2025Article
- Brainstem Glioma Prognostication: Static FET PET/CT.Cancers · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High-grade glioma (HGG) is the most common cause of cancer death in children and the most common primary central nervous system tumor in adults. While pediatric HGG was once thought to be biologically similar to the adult form of disease, research has shown these malignancies to be significantly molecularly distinct, necessitating distinct approaches to their clinical management. However, emerging data have shown shared molecular events in pediatric and adult HGG including the histone H3K27M mutation. This somatic missense mutation occurs in genes encoding one of two isoforms of the Histone H3 protein, H3F3A (H3.3), or HIST1H3B (H3.1), and is detected in up to 80% of pediatric diffuse midline gliomas and in up to 60% of adult diffuse gliomas. Importantly, the H3K27M mutation is associated with poorer overall survival and response to therapy compared to patients with H3 wild-type tumors. Here, we review the clinical features and biological underpinnings of pediatric and adult H3K27M mutant glioma, offering a groundwork for understanding current research and clinical approaches for the care of patients suffering with this challenging disease.
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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.