ReviewBrain pathology (Zurich, Switzerland)2013
Chromatin remodeling defects in pediatric and young adult glioblastoma: a tale of a variant histone 3 tail.
Review in Brain pathology (Zurich, Switzerland), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis 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.
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
58 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Thalamic gliomas in adults: a systematic review of clinical characteristics, treatment strategies, and survival outcomes.Journal of neuro-oncology · 2021Pooled it
- The potential role of miR-34a and miR-34c in the regulation of pediatric high-grade glioma 4 aggressiveness.Pediatric research · 2026Article
- Personalized survival prediction in pediatric glioblastoma using a machine learning-powered web tool.Translational cancer research · 2026Article
- Circulating miRNAs as potential liquid biomarkers for pediatric gliomas.Pediatric research · 2026Article
- Promising efficacy of teniposide in H3K27M mutant diffuse midline gliomas: a case report.Frontiers in oncology · 2026Article
- Hyperpolarized Carbon-13 Metabolic Imaging Differentiates Distinctive Molecular Phenotypes in Diffuse Midline Gliomas.Molecules (Basel, Switzerland) · 2025Article
- What Epigenetics Teaches Us About Neuron-Glioma Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Imaging features and consideration of progression pattern of diffuse hemispheric gliomas, H3 G34-mutant.Acta neuropathologica communications · 2025Article
- Unravelling the mosaic: Epigenetic diversity in glioblastoma.Molecular oncology · 2024Review
- Multimodal magnetic resonance imaging (MRI) of juvenile and adult diffuse hemispheric gliomas with H3 G34-mutation: a case description.Quantitative imaging in medicine and surgery · 2024Article
- Article
- Epigenetics to clinicopathological features: a bibliometric analysis of H3 G34-mutant diffuse hemispheric glioma literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024Review
- Rewiring of the promoter-enhancer interactome and regulatory landscape in glioblastoma orchestrates gene expression underlying neurogliomal synaptic communication.Nature communications · 2023Article
- Super-enhancer hijacking drives ectopic expression of hedgehog pathway ligands in meningiomas.Nature communications · 2023Article
- Magnetic Resonance Imaging Characteristics of Molecular Subgroups in Pediatric H3 K27M Mutant Diffuse Midline Glioma.Clinical neuroradiology · 2022Article
- Review
- The Role of MacroH2A Histone Variants in Cancer.Cancers · 2021Review
- Mapping chromatin accessibility and active regulatory elements reveals pathological mechanisms in human gliomas.Nature communications · 2021Article
- Diffuse midline glioma with H3 K27M-mutation in an 83-year-old woman.CNS oncology · 2021Article
- Cryo-EM structure of SETD2/Set2 methyltransferase bound to a nucleosome containing oncohistone mutations.Cell discovery · 2021Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Primary brain tumors occur in 8 out of 100 000 people and are the leading cause of cancer-related death in children. Among brain tumors, high-grade astrocytomas (HGAs) including glioblastoma multiforme (GBM) are aggressive and are lethal human cancers. Despite decades of concerted therapeutic efforts, HGAs remain essentially incurable in adults and children. Recent discoveries have revolutionized our understanding of these tumors in children and young adults. Recurrent somatic driver mutations in the tail of histone 3 variant 3 (H3.3), leading to amino acid substitutions at key residues, namely lysine (K) 27 (K27M) and glycine 34 (G34R/G34V), were identified as a new molecular mechanism in pediatric GBM. These mutations represent the pediatric counterpart of the recurrent mutations in isocitrate dehydrogenases (IDH) identified in young adult gliomas and provide a much-needed new pathway that can be targeted for therapeutic development. This review will provide an overview of the potential role of these mutations in altering chromatin structure and affecting specific molecular pathways ultimately leading to gliomagenesis. The distinct changes in chromatin structure and the specific downstream events induced by each mutation need characterizing independently if progress is to be made in tackling this devastating cancer.
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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.