ArticleCell cycle (Georgetown, Tex.)2013
A lesson learned from the H3.3K27M mutation found in pediatric glioma: a new approach to the study of the function of histone modifications in vivo?
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- SETD8-mediated mono-methylation of YAP at K76 promotes K48-linked polyubiquitination and degradation to suppress colorectal cancer.Cell death and differentiation · 2026Article
- H2BE113K mutation promotes breast cancer metastasis through modulating chromatin dynamics.Science advances · 2026Article
- Stapled histone H3 tails are super-substrates for lysine methyltransferase SETD7.Chemical science · 2026Article
- Current Landscape of Preclinical Models for Pediatric Gliomas: Clinical Implications and Future Directions.Cancers · 2025Review
- Single amino acid mutations in histone H3.3 illuminate the functional significance of H3K4 methylation in plants.Nature communications · 2025Article
- Phenotypic and Functional Characterization of Oncohistone Mutations in Breast Cancers.bioRxiv : the preprint server for biology · 2025Article
- Leveraging dominant-negative histone H3 K-to-M mutations to study chromatin during differentiation and development.Development (Cambridge, England) · 2023Review
- Review
- Histone 3 Methyltransferases Alter Melanoma Initiation and Progression Through Discrete Mechanisms.Frontiers in cell and developmental biology · 2022Article
- Histone H2B Mutations in Cancer.Biomedicines · 2021Review
- The histone H3K9M mutation synergizes with H3K14 ubiquitylation to selectively sequester histone H3K9 methyltransferase Clr4 at heterochromatin.Cell reports · 2021Article
- The incorporation loci of H3.3K36M determine its preferential prevalence in chondroblastomas.Cell death & disease · 2021Article
- Biophysical and epigenetic regulation of cancer stemness, invasiveness and immune action.Current tissue microenvironment reports · 2020Article
- Reciprocal H3.3 gene editing identifies K27M and G34R mechanisms in pediatric glioma including NOTCH signaling.Communications biology · 2020Article
- Inhibition of Glioma Cells' Proliferation by Doxorubicin-Loaded Exosomes via Microfluidics.International journal of nanomedicine · 2020Article
- Adult H3K27M-mutant diffuse midline glioma with gliomatosis cerebri growth pattern: Case report and review of the literature.International journal of surgery case reports · 2020Article
- Oncohistone Mutations in Diffuse Intrinsic Pontine Glioma.Trends in cancer · 2019Review
- Spinal cord high-grade infiltrating gliomas in adults: clinico-pathological and molecular evaluation.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
- Epigenetics as a New Frontier in Orthopedic Regenerative Medicine and Oncology.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019Review
- H3.3K4M destabilizes enhancer H3K4 methyltransferases MLL3/MLL4 and impairs adipose tissue development.Nucleic acids research · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor in human. Recent studies on high-grade pediatric GBM have identified two recurrent mutations (K27M and G34R/V) in genes encoding histone H3 (H3F3A for H3.3 and HIST1H3B for H3.1). The two histone H3 mutations are mutually exclusive and give rise to tumors in different brain compartments. Recently, we and others have shown that the histone H3 K27M mutation specifically altered the di- and tri-methylation of endogenous histone H3 at Lys27. Genome-wide studies using ChIP-seq on H3.3K27M patient samples indicate a global reduction of H3K27me3 on chromatin. Remarkably, we also found a dramatic enrichment of H3K27me3 and EZH2 (the catalytic subunit H3K27 methyltransferase) at hundreds of gene loci in H3.3K27M patient cells. Here, we discuss potential mechanisms whereby H3K27me3 is enriched at chromatin loci in cells expressing the H3.3K27M mutation and report effects of Lys-to-Met mutations of other well-studied lysine residues of histone H3.1/H3.3 and H4 on the corresponding endogenous lysine methylation. We suggest that mutation(s) on histones may be found in a variety of human diseases, and the expression of mutant histones may help to address the function of histone lysine methylation and possibly other modifications in mammalian cells.
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