ArticleNucleic acids research2024
Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- G34R cancer mutation alters the conformational ensemble and dynamics of the histone H3.3 tails.Nucleic acids research · 2026Article
- A review of diffuse hemispheric glioma, H3 G34-mutant disease development, DNA repair, microenvironment, and treatments on the horizon.NPJ precision oncology · 2025Review
- IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- H3.1K27M-induced misregulation of the TONSOKU-H3.1 pathway causes genomic instability.Nature communications · 2025Article
- PALB2 deficiency may sensitize H3K27M-mutant pediatric HGG cells to BMN673/talazoparib.Frontiers in oncology · 2025Article
- DNMT1 prolonged absence is a tunable cellular stress that triggers cell proliferation arrest to protect from major DNA methylation loss.Cellular and molecular life sciences : CMLS · 2024Article
- CDK-dependent phosphorylation regulates PNKP function in DNA replication.The Journal of biological chemistry · 2024Article
- Histone H3 mutations and their impact on genome stability maintenance.Biochemical Society transactions · 2024Review
- Review
- Emerging roles of cancer-associated histone mutations in genomic instabilities.Frontiers in cell and developmental biology · 2024Review
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
- A scoping review of diffuse hemispheric glioma, H3 G34-mutant: Epigenetic and molecular profiles, clinicopathology, and treatment avenues.Neuro-oncology advancesArticle
Corrections and comments
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Authors and funding
28 authors at 8 institutions in 4 countries.
Funding
Abstract
Pediatric high-grade gliomas (pHGG) are devastating and incurable brain tumors with recurrent mutations in histone H3.3. These mutations promote oncogenesis by dysregulating gene expression through alterations of histone modifications. We identify aberrant DNA repair as an independent mechanism, which fosters genome instability in H3.3 mutant pHGG, and opens new therapeutic options. The two most frequent H3.3 mutations in pHGG, K27M and G34R, drive aberrant repair of replication-associated damage by non-homologous end joining (NHEJ). Aberrant NHEJ is mediated by the DNA repair enzyme polynucleotide kinase 3'-phosphatase (PNKP), which shows increased association with mutant H3.3 at damaged replication forks. PNKP sustains the proliferation of cells bearing H3.3 mutations, thus conferring a molecular vulnerability, specific to mutant cells, with potential for therapeutic targeting.
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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.