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Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
EZH2 is a potential therapeutic target for H3K27M mutant paediatric gliomas
PubMed Similar studies
EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [RNA-Seq]
PubMed Similar studies SRA Run Selector
EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [ChIP-seq]
Multiple modes of PRC2 inhibition elicit global chromatin alterations in H3K27M pediatric glioma
Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG
Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [RNA-seq]
Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [ChIP-seq]
H3.3K27M mutant proteins reprogram epigenome by sequestering the PRC2 complex to poised enhancers
PubMed Full text in PMC Similar studies SRA Run Selector
Transcriptional dependencies in diffuse intrinsic pontine glioma
H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [RNA-seq]
H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation
PubMed Full text in PMC Similar studies
H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [WGBS]
H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [ChIP-seq]
Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ChIP-Seq 2]
Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ChIP-Seq]
Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas
Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ATAC-seq]
Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [RNA-Seq]
Variant and cell-context specific H3K27M reprogramming results in distinct enhancer architecture and oncogenic states
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