ArticleeLife2021
Surprising phenotypic diversity of cancer-associated mutations of Gly 34 in the histone H3 tail.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 36 citations in OpenAlex.
- Integrated high-resolution copy number and histomolecular analysis of diffuse hemispheric glioma, H3 G34-mutant reveals universal TP53 abnormalities.Brain pathology (Zurich, Switzerland) · 2026Article
- Cancer histone H2A.Z missense mutations disrupt function through distinct local and allosteric effects.Research square · 2026Article
- The clinical and molecular landscape of diffuse hemispheric glioma, H3 G34-mutant.Neuro-oncology · 2025Article
- Histone H3E50K remodels chromatin to confer oncogenic activity and support an EMT phenotype.NAR cancer · 2025Article
- Oncohistone H3 E97K mutation facilitates CENP-A mislocalization and chromosomal instability in budding yeast.Nucleic acids research · 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
- (B)On(e)-cohistones and the epigenetic alterations at the root of bone cancer.Cell death and differentiation · 2025Review
- Epigenetic reprogramming in pediatric gliomas: from molecular mechanisms to therapeutic implications.Trends in cancer · 2024Review
- Histone H3 mutations and their impact on genome stability maintenance.Biochemical Society transactions · 2024Review
- Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.Nucleic acids research · 2024Article
- HIRA vs. DAXX: the two axes shaping the histone H3.3 landscape.Experimental & molecular medicine · 2024Review
- Emerging roles of cancer-associated histone mutations in genomic instabilities.Frontiers in cell and developmental biology · 2024Review
- Exploring the Molecular Underpinnings of Cancer-Causing Oncohistone Mutants Using Yeast as a Model.Journal of fungi (Basel, Switzerland) · 2023Review
- Review
- Article
- Oncohistones and disrupted development in pediatric-type diffuse high-grade glioma.Cancer metastasis reviews · 2023Review
- H3G34-mutant diffuse hemispheric glioma with osseous metastases: a case report and literature review.CNS oncology · 2023Review
- Diagnostic value ofJournal of bone oncology · 2023Article
- H3.3-G34 mutations impair DNA repair and promote cGAS/STING-mediated immune responses in pediatric high-grade glioma models.The Journal of clinical investigation · 2022Article
- A Saccharomyces cerevisiae model and screen to define the functional consequences of oncogenic histone missense mutations.G3 (Bethesda, Md.) · 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
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Sequencing of cancer genomes has identified recurrent somatic mutations in histones, termed oncohistones, which are frequently poorly understood. Previously we showed that fission yeast expressing only the H3.3G34R mutant identified in aggressive pediatric glioma had reduced H3K36 trimethylation and acetylation, increased genomic instability and replicative stress, and defective homology-dependent DNA damage repair. Here we show that surprisingly distinct phenotypes result from G34V (also in glioma) and G34W (giant cell tumors of bone) mutations, differentially affecting H3K36 modifications, subtelomeric silencing, genomic stability; sensitivity to irradiation, alkylating agents, and hydroxyurea; and influencing DNA repair. In cancer, only 1 of 30 alleles encoding H3 is mutated. Whilst co-expression of wild-type H3 rescues most G34 mutant phenotypes, G34R causes dominant hydroxyurea sensitivity, homologous recombination defects, and dominant subtelomeric silencing. Together, these studies demonstrate the complexity associated with different substitutions at even a single residue in H3 and highlight the utility of genetically tractable systems for their analysis.
Indexed as
Identifiers
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.