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Links from GEO DataSets

Items: 20

1.

EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [ChIP-seq]

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive brain tumour that is located in the pons and primarily affects children. Whole-exome sequencing studies have identified recurrent driver mutations in H3F3A and HIST1H3B, leading to the expression of histone H3 in which lysine 27 is substituted with methionine (H3K27M) in nearly 80% of DIPGs. H3K27M has been shown to inhibit Polycomb Repressive Complex 2 (PRC2) activity by binding to its catalytic subunit EZH2, and although DIPGs with H3K27M mutation show global loss of H3 with trimethylated lysine 27 (H3K27me3), several genes retain H3K27me3. more...
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL13112
13 Samples
Download data: BW, TXT
Series
Accession:
GSE71225
ID:
200071225
2.

EZH2 is a potential therapeutic target for H3K27M mutant paediatric gliomas

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL17021
38 Samples
Download data: BED, BW
Series
Accession:
GSE85390
ID:
200085390
3.

EZH2 inhibition as a targeted therapy for H3K27M mutant pediatric gliomas [RNA-Seq]

(Submitter supplied) Diffuse intrinsic pontine glioma (DIPG) is a highly aggressive brain tumour that is located in the pons and primarily affects children. Whole-exome sequencing studies have identified recurrent driver mutations in H3F3A and HIST1H3B, leading to the expression of histone H3 in which lysine 27 is substituted with methionine (H3K27M) in nearly 80% of DIPGs. H3K27M inhibits Polycomb Repressive Complex 2 (PRC2) activity by binding to its catalytic subunit EZH2 and although DIPGs with H3K27M mutation show global loss of H3 with trimethylated lysine 27 (H3K27me3), several genomic loci are still H3K27me3 positive. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: BW
Series
Accession:
GSE71387
ID:
200071387
4.

Heterotypic nucleosomes and PRC2 drive DIPG oncogenesis

(Submitter supplied) Diffuse intrinsic pontine gliomas (DIPG) are characterized by a heterozygous lysine-to-methionine mutation of histone H3 (H3K27M) that potently reduces Polycomb Repressive Complex 2 (PRC2) methylation of wild-type histone H3K27 (H3K27wt). The role of H3K27M and reduced H3K27wt methylation in DIPG pathogenesis has yet to be determined. Here, we have performed epigenomic profiling of patient-derived H3K27M mutant DIPG cells and demonstrate that H3K27M resides in nucleosomes with H3K27wt acetylation (H3K27ac), and H3K27M-H3K27ac containing nucleosomes co-localize with bromodomain proteins at actively transcribed genes and that PRC2 is excluded from H3K27M occupied regions. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
100 Samples
Download data: BW
5.

RNAseq analysis of murine brainstem gliomas with and without H3.3K27M

(Submitter supplied) Using the RCAS/tv-a system, we induced murine brainstem gliomas (PDGF-B; p53 loss using RCAS-Cre with and without H3.3K27M) in Nestin tv-a; p53 floxed mice
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL9185
6 Samples
Download data: XLSX
Series
Accession:
GSE98765
ID:
200098765
6.

Multiple modes of PRC2 inhibition elicit global chromatin alterations in H3K27M pediatric glioma

(Submitter supplied) A methionine substitution at lysine 27 on histone H3 variants (H3K27M) characterizes ~80% of diffuse intrinsic pontine gliomas (DIPG) and inhibits PRC2 in a dominant negative fashion. Yet, the mechanisms for this inhibition and abnormal epigenomic landscape have not been resolved. Using quantitative proteomics, we discovered that robust PRC2 inhibition requires levels of H3K27M greatly exceeding those of PRC2, seen in DIPG. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
64 Samples
Download data: BW
7.

Epigenetic changes in mouse neuronal stem cells and human DIPG cells with histone H3K27M mutations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL19057 GPL18573
16 Samples
Download data
Series
Accession:
GSE135419
ID:
200135419
8.

Epigenetic changes in human DIPG cells with histone H3K27M mutations [ATAC-seq]

(Submitter supplied) We assessed changes in chromatin accessibility in H3.3K27M DIPG cell lines on knockdown of metabolic enzymes including HK2, GDH and IDH1
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: CSV
Series
Accession:
GSE135418
ID:
200135418
9.

Epigenetic changes in mouse neuronal stem cells with histone H3K27M mutations [ChIP-seq]

(Submitter supplied) H3.3K27M mutations or H3.3 WT were expressed in in neuronal stem cells (Nsc) derived from p16Ink4a/p14Arf knockout (KO) animal. Genomic changes in H3K27me3, H3K27ac and H3K4me3 were assessed between H3.3K27M and H3.3WT cells.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
8 Samples
Download data: XLSX
Series
Accession:
GSE135417
ID:
200135417
10.

Gene expression profiling of two DLBCL cell lines upon shRNA mediated knockdown of EZH2

(Submitter supplied) We studied transcriptional changes by Affymetrix human microarrays in 2 DLBCL cell lines as a result of shRNA mediated knockdown of EZH2. In eukaryotes, epigenetic post-translational modification of histones is critical for regulation of chromatin structure and gene expression. EZH2 is the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2) and is responsible for repressing target gene expression through methylation of histone H3 on lysine 27 (H3K27). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
6 Samples
Download data: CEL
Series
Accession:
GSE41239
ID:
200041239
11.

EZH2 Inhibition as a Therapeutic Strategy for Lymphoma with EZH2 Activating Mutations

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by array
Platforms:
GPL570 GPL9115
52 Samples
Download data: BED, CEL
Series
Accession:
GSE40972
ID:
200040972
12.

Gene expression profiling of EZH2 mutant and wild type DLBCL cell lines treated with EZH2 inhibitor

(Submitter supplied) We studied transcriptional changes by Affymetrix human microarrays in DLBCL cell lines as a result of treatment with GSK126, a potent, highly-selective, SAM-competitive, small molecule inhibitor of EZH2 In eukaryotes, epigenetic post-translational modification of histones is critical for regulation of chromatin structure and gene expression. EZH2 is the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2) and is responsible for repressing target gene expression through methylation of histone H3 on lysine 27 (H3K27). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
40 Samples
Download data: CEL
Series
Accession:
GSE40971
ID:
200040971
13.

ChIP-seq analysis of H3K27me3 histone modification in EZH2 mutant and wild type DLBCL cell lines

(Submitter supplied) In eukaryotes, epigenetic post-translational modification of histones is critical for regulation of chromatin structure and gene expression. EZH2 is the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2) and is responsible for repressing target gene expression through methylation of histone H3 on lysine 27 (H3K27). Over-expression of EZH2 is implicated in tumorigenesis and correlates with poor prognosis in multiple tumor types. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL9115
6 Samples
Download data: BED
Series
Accession:
GSE40970
ID:
200040970
14.

Targeting SWI/SNF ATPases in H3.3K27M Diffuse Intrinsic Pontine Gliomas

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
8 Samples
Download data: BW
Series
Accession:
GSE229454
ID:
200229454
15.

Targeting SWI/SNF ATPases in H3.3K27M Diffuse Intrinsic Pontine Gliomas [ATAC-Seq]

(Submitter supplied) Diffuse midline gliomas (DMGs), including diffuse intrinsic pontine gliomas (DIPGs), bearing lysine-to-methionine mutations in histone H3 at lysine 27 (H3K27M) are lethal childhood brain cancers. These tumors harbor a global reduction in the transcriptional repressive mark H3K27me3 accompanied by an increase in the transcriptional activation mark H3K27ac. We postulated that H3K27M mutations, in addition to altering H3K27 modifications, reprogram the master chromatin remodeling SWI/SNF complex. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: BW
Series
Accession:
GSE229453
ID:
200229453
16.

Targeting SWI/SNF ATPases in H3.3K27M Diffuse Intrinsic Pontine Gliomas [RNA-Seq]

(Submitter supplied) Diffuse midline gliomas (DMGs), including diffuse intrinsic pontine gliomas (DIPGs), bearing lysine-to-methionine mutations in histone H3 at lysine 27 (H3K27M) are lethal childhood brain cancers. These tumors harbor a global reduction in the transcriptional repressive mark H3K27me3 accompanied by an increase in the transcriptional activation mark H3K27ac. We postulated that H3K27M mutations, in addition to altering H3K27 modifications, reprogram the master chromatin remodeling SWI/SNF complex. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: TXT
Series
Accession:
GSE229452
ID:
200229452
17.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
30 Samples
Download data: BED, BIGWIG, TXT
Series
Accession:
GSE110572
ID:
200110572
18.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [RNA-seq]

(Submitter supplied) Histone H3 lysine 27 to methionine mutations (H3K27M) resulting in aberrant chromatin regulation are frequently observed in Diffuse Intrinsic Pontine Glioma (DIPG), a pediatric brain tumor with no cure. We conducted a CRISPR screen to determine if various chromatin regulators might be targeted to treat DIPG. Excitingly, this genetic screen reveals that co-targeting lysine specific demethylase 1 (LSD1) and histone deacetylases (HDACs) results in an enhanced growth suppressive effect in patient DIPG cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE110571
ID:
200110571
19.

Re-programing chromatin with a bifunctional LSD1/HDAC inhibitor induces therapeutic differentiation in DIPG [ChIP-seq]

(Submitter supplied) Histone H3 lysine 27 to methionine mutations (H3K27M) resulting in aberrant chromatin regulation are frequently observed in Diffuse Intrinsic Pontine Glioma (DIPG), a pediatric brain tumor with no cure. We conducted a CRISPR screen to determine if various chromatin regulators might be targeted to treat DIPG. Excitingly, this genetic screen reveals that co-targeting lysine specific demethylase 1 (LSD1) and histone deacetylases (HDACs) results in an enhanced growth suppressive effect in patient DIPG cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
18 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE110570
ID:
200110570
20.

H3.3 K27M depletion increases differentiation and extends latency of diffuse intrinsic pontine glioma growth in vivo

(Submitter supplied) Xenografts from human pediatric brainstem gliomas bearing K27M in H3F3A were transduced with non silencing or H3F3A shRNA to assess the impact of the K27M on tumor growth, gene expression and epigenetics
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL16791 GPL20301
130 Samples
Download data: BED, BW, NARROWPEAK
Series
Accession:
GSE115875
ID:
200115875
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