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TranscriptomicsHuman ESC-based modeling of pediatric gliomas by K27M mutation in histone H3.3 variant
Human diffuse intrinsic pontine gliomas (DIPG) are an aggressive form of pediatric brain tumors that arise in the pons in young children thus resulting in significant morbidity and very poor survival. Recent data suggest that mutations in the histone H3.3 variant are often found in these tumors, tho...
ORGANISM(S): Homo sapiens 
2014-11-21 | E-GEOD-55541 | biostudies-arrayexpress
ProteomicsAberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors
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, whi...
ORGANISM(S): Homo sapiens (Human) 
2024-01-10 | PXD041132 | Pride
Dna repair Brain cancer Non-homologous end joining Pnkp Dna damage Pediatric high-grade glioma Replication fork Oncohistone 
TranscriptomicsGene expression data of pHGG tumor samples
Pediatric high-grade gliomas (pHGGs) harboring the K27M mutation of H3F3A (histone H3.3) are characterized by global reduction of the repressive histone mark H3K27me3 and DNA hypomethylation. Analysis of K27M-induced changes on H3K27me3 occupancy and DNA methylation at differentially expresed genes ...
ORGANISM(S): Homo sapiens 
2014-05-14 | E-GEOD-49822 | biostudies-arrayexpress
TranscriptomicsThe histone H3.3K27M mutation in pediatric glioma reprograms H3K27 methylation and gene expression
Recent studies have identified a Lys 27-to-methionine (K27M) mutation at one allele of H3F3A, one of the two genes encoding histone H3 variant H3.3, in 60% of high-grade pediatric glioma cases. The median survival of this group of patients after diagnosis is ∼1 yr. Here we show that the levels of H3...
ORGANISM(S): Homo sapiens 
2014-09-20 | E-GEOD-61586 | biostudies-arrayexpress
UnknownThe histone H3.3 K27M mutation suppresses Ser31phosphorylation and mitotic fidelity, which can directly drive gliomagenesis.
Not available
S-EPMC12673919 | biostudies-literature
UnknownHistone H3.3 K27M Accelerates Spontaneous Brainstem Glioma and Drives Restricted Changes in Bivalent Gene Expression.
Not available
S-EPMC6570409 | biostudies-literature
UnknownIdentification of genes functionally involved in the detrimental effects of mutant histone H3.3-K27M in Drosophila melanogaster.
Not available
S-EPMC6502498 | biostudies-literature
GenomicsSpontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects
Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects
PRJNA720937 | ENA
GenomicsPaediatric Glioma Histone H3.3 K27M/G34R Mutations Drive Abnormalities in Phase-Separated PML Nuclear Bodies.
Paediatric Glioma Histone H3.3 K27M/G34R Mutations Drive Abnormalities in Phase-Separated PML Nuclear Bodies.
PRJNA864751 | ENA
UnknownReciprocal H3.3 gene editing identifies K27M and G34R mechanisms in pediatric glioma including NOTCH signaling.
Not available
S-EPMC7347881 | biostudies-literature
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