ReviewCancers2019
Histone H3 Mutations: An Updated View of Their Role in Chromatin Deregulation and Cancer.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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
76 citing papers in PubMed, 121 citations in OpenAlex.
- Plasma histone monomers as novel diagnostic markers in adult glioblastoma.The journal of liquid biopsy · 2026Article
- A new hope: Clinical advances in targeted therapies for pediatric diffuse midline glioma.Neuro-oncology advances · 2026Review
- Illuminating radiogenomic signatures in pediatric-type diffuse gliomas: insights into molecular, clinical, and imaging correlations. Part I: high-grade group.La Radiologia medica · 2025Review
- Engineered histones reshape chromatin in human cells.bioRxiv : the preprint server for biology · 2025Article
- Review
- Exogenous expression of a histone H3.3 isoform causes extranuclear divisions in thebioRxiv : the preprint server for biology · 2025Article
- Characterization of oncohistone H2B variants in Schizosaccharomyces pombe reveals a key role of H2B monoubiquitination deficiency in genomic instability by altering gene expression.FEMS yeast research · 2025Article
- Diffuse midline gliomas, H3K27M-altered, of the pineal gland: the first synaptophysin-positive case and a systematic review.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025Review
- Histone H3 mutations and their impact on genome stability maintenance.Biochemical Society transactions · 2024Review
- A First-in-Class High-Throughput Screen to Discover Modulators of the Alternative Lengthening of Telomeres (ALT) Pathway.ACS pharmacology & translational science · 2024Article
- Review
- 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
- The 2021 World Health Organization Central Nervous System Tumor Classification: The Spectrum of Diffuse Gliomas.Biomedicines · 2024Review
- The Landscape of Pediatric High-Grade Gliomas: The Virtues and Pitfalls of Pre-Clinical Models.Biology · 2024Review
- Periosteal chondroblastoma of the femoral neck: two cases and a review of the literature.Skeletal radiology · 2024Review
- ONC201 (Dordaviprone) in Recurrent H3 K27M-Mutant Diffuse Midline Glioma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Article
- Tertiary Amine Coupling by Oxidation for Selective Labeling of Dimethyl Lysine Post-Translational Modifications.Journal of the American Chemical Society · 2024Article
- Review
- Integration of histone modification-based risk signature with drug sensitivity analysis reveals novel therapeutic strategies for lower-grade glioma.Frontiers in pharmacology · 2024Article
- Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
In this review, we describe the attributes of histone H3 mutants identified in cancer. H3 mutants were first identified in genes encoding H3.3, in pediatric high-grade glioma, and subsequently in chondrosarcomas and giant cell tumors of bone (GCTB) in adolescents. The most heavily studied are the lysine to methionine mutants K27M and K36M, which perturb the target site for specific lysine methyltransferases and dominantly perturb methylation of corresponding lysines in other histone H3 proteins. We discuss recent progress in defining the consequences of these mutations on chromatin, including a newly emerging view of the central importance of the disruption of H3K36 modification in many distinct K to M histone mutant cancers. We also review new work exploring the role of H3.3 G34 mutants identified in pediatric glioma and GCTB. G34 is not itself post-translationally modified, but G34 mutation impinges on the modification of H3K36. Here, we ask if G34R mutation generates a new site for methylation on the histone tail. Finally, we consider evidence indicating that histone mutations might be more widespread in cancer than previously thought, and if the perceived bias towards mutation of H3.3 is real or reflects the biology of tumors in which the histone mutants were first identified.
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What OpenQuestion holds
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.