ArticleNAR cancer2025
Histone H3E50K remodels chromatin to confer oncogenic activity and support an EMT phenotype.
Article in NAR cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Epigenetic regulation of metabolism in Saccharomyces cerevisiae: mechanisms, metabolic crosstalk, and engineering applications.Molecular biology reports · 2026Review
- 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
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18 authors.
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Abstract
Sequencing of human patient tumors has identified recurrent missense mutations in genes encoding core histones. We report that mutations that convert histone H3 amino acid 50 from a glutamate to a lysine (H3E50K) support an oncogenic phenotype. Expression of H3E50K is sufficient to transform human cells as evidenced by an increase in cell migration and invasion, and an increase in proliferation and clonogenicity. H3E50K also increases the invasive phenotype in the context of co-occurring
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