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Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG
PubMed Similar studies
Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [RNA-seq]
PubMed Similar studies SRA Run Selector
Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [ChIP-seq]
Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo
PubMed Full text in PMC Similar studies
H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo [RNA-Seq]
H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo [ChIP-Seq]
PubMed Full text in PMC Similar studies SRA Run Selector
Transcriptional dependencies in diffuse intrinsic pontine glioma
Effect of CBL0137 on DIPG cells
PubMed Similar studies Analyze with GEO2R
Combination of CBL0137 and Panobinostat in DIPG
Potent anti-tumor efficacy of palbociclib in H3K27M-mutant diffuse intrinsic pontine glioma
RNA expression in MDA-MB-231 cells transfected with scramble, LSD1 or HDAC5 shRNA (HG-U133A_2)
PubMed Full text in PMC Similar studies Analyze with GEO2R
RNA expression in MDA-MB-231 cells treated for 24h with SAHA, Pargyline, or both [HG-U133A_2]
EZH2 is a potential therapeutic target for H3K27M mutant paediatric gliomas
EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [RNA-Seq]
EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [ChIP-seq]
RNAseq analysis of murine brainstem gliomas with and without H3.3K27M
Spontaneous 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 [RNA-seq]
Spontaneous DIPG Modeling Reveals Novel H3.3 K27M-Mediated Oncogenic Mechanisms Acting Through Epigenetic Effects [ChIP-seq]
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