ArticleActa neuropathologica communications2020
H3F3A mutant allele specific imbalance in an aggressive subtype of diffuse midline glioma, H3 K27M-mutant.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 51 citations in OpenAlex.
- Comparative analysis of clinical characteristics and prognostic factors in adult and pediatric patients with H3K27M-mutant diffuse midline glioma.Neurosurgical review · 2026Article
- Metabolic, perfusion, and diffusion imaging enhance diagnosis and prognosis of H3K27-altered diffuse midline gliomas.BMC medicine · 2025Article
- Neuroradiological, genetic and clinical characteristics of histone H3 K27-mutant diffuse midline gliomas in the Kansai Molecular Diagnosis Network for CNS Tumors (Kansai Network): multicenter retrospective cohort.Acta neuropathologica communications · 2024Article
- DNA Methylation Profiles Are Stable in H3 K27M-Mutant Diffuse Midline Glioma Neurosphere Cell Lines.Children (Basel, Switzerland) · 2024Article
- Full-length isoform concatenation sequencing to resolve cancer transcriptome complexity.BMC genomics · 2024Article
- Targeted detection of sequence variants in cell-free DNA from cerebrospinal fluid in pediatric central nervous system tumors.Frontiers in oncology · 2024Review
- Differences in survival prognosticators between children and adults with H3K27M-mutant diffuse midline glioma.CNS neuroscience & therapeutics · 2023Article
- Somatic Copy Number Alteration in Circulating Tumor DNA for Monitoring of Pediatric Patients with Cancer.Biomedicines · 2023Article
- Article
- Molecular diagnostics helps to identify distinct subgroups of spinal astrocytomas.Acta neuropathologica communications · 2021Article
- Global activation of oncogenic pathways underlies therapy resistance in diffuse midline glioma.Acta neuropathologica communications · 2020Article
- Clinical Features and Molecular Markers on Diffuse Midline Gliomas With H3K27M Mutations: A 43 Cases Retrospective Cohort Study.Frontiers in oncology · 2020Article
- A scoping review of diffuse hemispheric glioma, H3 G34-mutant: Epigenetic and molecular profiles, clinicopathology, and treatment avenues.Neuro-oncology advancesArticle
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22 authors at 5 institutions in 1 country.
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Abstract
Diffuse midline glioma, H3 K27M-mutant is a lethal brain tumor located in the thalamus, brain stem, or spinal cord. H3 K27M encoded by the mutation of a histone H3 gene such as H3F3A plays a pivotal role in the tumorigenesis of this type of glioma. Although several studies have revealed comprehensive genetic and epigenetic profiling, the prognostic factors of these tumors have not been identified to date. In various cancers, oncogenic driver genes have been found to exhibit characteristic copy number alterations termed mutant allele specific imbalance (MASI). Here, we showed that several diffuse midline glioma, H3 K27M-mutant exhibited high variant allele frequency (VAF) of the mutated H3F3A gene using droplet digital polymerase chain reaction (ddPCR) assays. Whole-genome sequencing (WGS) revealed that these cases had various copy number alterations that affected the mutant and/or wild-type alleles of the H3F3A gene. We also found that these MASI cases showed a significantly higher Ki-67 index and poorer survival compared with those in the lower VAF cases (P < 0.05). Our results indicated that the MASI of the H3F3A K27M mutation was associated with the aggressive phenotype of the diffuse midline glioma, H3 K27M-mutant via upregulation of the H3 K27M mutant protein, resulting in downregulation of H3K27me3 modification.
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