ReviewChromosoma2015
Histone H3 mutations--a special role for H3.3 in tumorigenesis?
Review in Chromosoma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Contribution of histone variants to aneuploidy: a cancer perspective.Frontiers in genetics · 2023Pooled it
- Plasma histone monomers as novel diagnostic markers in adult glioblastoma.The journal of liquid biopsy · 2026Article
- A novel iPSC model of Bryant-Li-Bhoj neurodevelopmental/neurodegenerative syndrome demonstrates the role of histone H3.3 in chromatin dynamics, neuronal differentiation, and maturation.Journal of translational medicine · 2026Article
- Vaccine therapy for pediatric high-grade glioma: current landscape, challenges, and future directions.Journal of neuro-oncology · 2026Review
- Phase 1 study of mebendazole therapy for refractory/progressive or recurrent pediatric brain tumors.Neuro-oncology practice · 2025Article
- What Epigenetics Teaches Us About Neuron-Glioma Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- A simplified preparation method for single-nucleus RNA-sequencing using long-term frozen brain tumor tissues.Scientific reports · 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
- Pediatric brain tumor patients display altered immune activation and reduced lymphopoiesis at the onset of disease.NPJ precision oncology · 2024Article
- 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
- Analysis of copy number variants detected by sequencing in spontaneous abortion.Molecular cytogenetics · 2024Article
- Emerging roles of cancer-associated histone mutations in genomic instabilities.Frontiers in cell and developmental biology · 2024Review
- Casting histone variants during mammalian reproduction.Chromosoma · 2023Review
- H3 G34-mutant high-grade gliomas: integrated clinical, imaging and pathological characterisation of a single-centre case series.Acta neurochirurgica · 2023Article
- Small and Large Extracellular Vesicles Derived from Pleural Mesothelioma Cell Lines Offer Biomarker Potential.Cancers · 2023Article
- PRC2-independent actions of H3.3K27M in embryonic stem cell differentiation.Nucleic acids research · 2023Article
- Article
- SETD2: from chromatin modifier to multipronged regulator of the genome and beyond.Cellular and molecular life sciences : CMLS · 2022Review
- Pediatric High Grade Glioma Classification Criteria and Molecular Features of a Case Series.Genes · 2022Article
- Pediatric glioblastoma cells are sensitive to drugs that inhibit eIF2α dephosphorylation and its phosphomimetic S51D variant.Frontiers in oncology · 2022Article
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 1 institution in 1 country.
Funding
Abstract
Brain tumors are the most common solid tumors in children. Pediatric high-grade glioma (HGG) accounts for ∼8-12 % of these brain tumors and is a devastating disease as 70-90 % of patients die within 2 years of diagnosis. The failure to advance therapy for these children over the last 30 years is largely due to limited knowledge of the molecular basis for these tumors and a lack of disease models. Recently, sequencing of tumor cells revealed that histone H3 is frequently mutated in pediatric HGG, with up to 78 % of diffuse intrinsic pontine gliomas (DIPGs) carrying K27M and 36 % of non-brainstem gliomas carrying either K27M or G34R/V mutations. Although mutations in many chromatin modifiers have been identified in cancer, this was the first demonstration that histone mutations may be drivers of disease. Subsequent studies have identified high-frequency mutation of histone H3 to K36M in chondroblastomas and to G34W/L in giant cell tumors of bone, which are diseases of adolescents and young adults. Interestingly, the G34 mutations, the K36M mutations, and the majority of K27M mutations occur in genes encoding the replacement histone H3.3. Here, we review the peculiar characteristics of histone H3.3 and use this information as a backdrop to highlight current thinking about how the identified mutations may contribute to disease development.
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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.