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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

EZH2 is a potential therapeutic target for H3K27M mutant paediatric gliomas

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL16791
38 Samples
Download data: BED, BW
Series
Accession:
GSE85390
ID:
200085390
4.

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
5.

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:
GPL13112 GPL11154
13 Samples
Download data: BW, TXT
Series
Accession:
GSE71225
ID:
200071225
6.

H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [RNA-seq]

(Submitter supplied) The discovery of H3K27M mutations in pediatric gliomas marked a new chapter in cancer epigenetics. Numerous studies have investigated the effect of this mutation on H3K27 trimethylation, but only recently have we started to realize its additional effects on the epigenome. Here, we use isogenic glioma H3K27M(+/-) cell lines to investigate H3K27 methylation and its interaction with H3K36 and H3K9 modifications. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
14 Samples
Download data: BW
7.

H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing; Expression profiling by high throughput sequencing
5 related Platforms
135 Samples
Download data: BW, TDF
Series
Accession:
GSE147783
ID:
200147783
8.

H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [WGBS]

(Submitter supplied) The discovery of H3K27M mutations in pediatric gliomas marked a new chapter in cancer epigenetics. Numerous studies have investigated the effect of this mutation on H3K27 trimethylation, but only recently have we started to realize its additional effects on the epigenome. Here, we use isogenic glioma H3K27M(+/-) cell lines to investigate H3K27 methylation and its interaction with H3K36 and H3K9 modifications. more...
Organism:
Homo sapiens
Type:
Methylation profiling by high throughput sequencing
Platforms:
GPL16791 GPL20795
7 Samples
Download data: TDF
Series
Accession:
GSE147782
ID:
200147782
9.

H3K27M in Gliomas Causes a One-step Decrease in H3K27 Methylation and Reduced Spreading Within the Constraints of H3K36 Methylation [ChIP-seq]

(Submitter supplied) The discovery of H3K27M mutations in pediatric gliomas marked a new chapter in cancer epigenetics. Numerous studies have investigated the effect of this mutation on H3K27 trimethylation, but only recently have we started to realize its additional effects on the epigenome. Here, we use isogenic glioma H3K27M(+/-) cell lines to investigate H3K27 methylation and its interaction with H3K36 and H3K9 modifications. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
114 Samples
Download data: BW
Series
Accession:
GSE147780
ID:
200147780
10.

Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ChIP-Seq 2]

(Submitter supplied) Epigenetic alterations are recurrently observed in cancer and are the subject of active therapeutic investigations. Midline high-grade gliomas (HGGs) are deadly brain tumors characterized by lysine-to-methionine substitutions at position 27 in histone 3 (H3) variants (denoted H3K27M), which are core components of the nucleosome. H3K27M, the first event in midline HGG development, results in a drastic loss of the repressive histone mark H3K27 tri-methylation (H3K27me3), and a notable increase in H3K27 acetylation (H3K27ac), a mark associated with active chromatin and cellular identity. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
4 related Platforms
22 Samples
Download data: TXT
Series
Accession:
GSE129136
ID:
200129136
11.

Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ChIP-Seq]

(Submitter supplied) Epigenetic alterations are recurrently observed in cancer and are the subject of active therapeutic investigations. Midline high-grade gliomas (HGGs) are deadly brain tumors characterized by lysine-to-methionine substitutions at position 27 in histone 3 (H3) variants (denoted H3K27M), which are core components of the nucleosome. H3K27M, the first event in midline HGG development, results in a drastic loss of the repressive histone mark H3K27 tri-methylation (H3K27me3), and a notable increase in H3K27 acetylation (H3K27ac), a mark associated with active chromatin and cellular identity. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
80 Samples
Download data: BED
Series
Accession:
GSE129135
ID:
200129135
12.

Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M 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
4 related Platforms
210 Samples
Download data: BED, NARROWPEAK
Series
Accession:
GSE128745
ID:
200128745
13.

Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [ATAC-seq]

(Submitter supplied) Epigenetic alterations are recurrently observed in cancer and are the subject of active therapeutic investigations. Midline high-grade gliomas (HGGs) are deadly brain tumors characterized by lysine-to-methionine substitutions at position 27 in histone 3 (H3) variants (denoted H3K27M), which are core components of the nucleosome. H3K27M, the first event in midline HGG development, results in a drastic loss of the repressive histone mark H3K27 tri-methylation (H3K27me3), and a notable increase in H3K27 acetylation (H3K27ac), a mark associated with active chromatin and cellular identity. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: NARROWPEAK
Series
Accession:
GSE128744
ID:
200128744
14.

Pervasive H3K27 acetylation leads to ERV expression and a therapeutic vulnerability in H3K27M gliomas [RNA-Seq]

(Submitter supplied) Epigenetic alterations are recurrently observed in cancer and are the subject of active therapeutic investigations. Midline high-grade gliomas (HGGs) are deadly brain tumors characterized by lysine-to-methionine substitutions at position 27 in histone 3 (H3) variants (denoted H3K27M), which are core components of the nucleosome. H3K27M, the first event in midline HGG development, results in a drastic loss of the repressive histone mark H3K27 tri-methylation (H3K27me3), and a notable increase in H3K27 acetylation (H3K27ac), a mark associated with active chromatin and cellular identity. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Other
Platforms:
GPL16791 GPL20301 GPL11154
96 Samples
Download data: TXT
15.

Jarid2 methylation is required for PRC2 functioning during ES cells differentiation

(Submitter supplied) We report that Jarid2 is methylated at K116 by the polycomb complex PRC2. We analyzed Jarid2 versus Methylated Jarid2 genomic localization by ChIP-seq. We also study H3K27 enrichment in Jarid2 knock out ES cells and in cells rescued for Jarid2 or a mutant that cannot be methylated. ChIP-seq for H3K27me3 was perfomed in undiffrentiated ES cells as well as after 8 days of diffrentiation toward Embroyid Bodies (Hanging Drop method).
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
16 Samples
Download data: BIGWIG, BROADPEAK, TXT
Series
Accession:
GSE55630
ID:
200055630
16.

The H3K36me2 writer-reader dependency in H3K27M-DIPG

(Submitter supplied) The lysine-to-methionine mutation at residue 27 of histone H3 (H3K27M) is a driving mutation in Diffuse Intrinsic Pontine Glioma (DIPG), a highly aggressive form of pediatric brain tumor with no effective treatment and little chance of survival. H3K27M reshapes the epigenome through a global inhibition of PRC2 catalytic activity, displacement of methylation at lysine 27 of histone H3 (H3K27me2/3), and thus promoting oncogenesis of DIPG. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
34 Samples
Download data: BW, TXT
17.

Capturing the onset of PRC2-mediated repressive domain formation[ChIP-Seq, 3]

(Submitter supplied) Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19057
19 Samples
Download data: BW
Series
Accession:
GSE109580
ID:
200109580
18.

Capturing the onset of PRC2-mediated repressive domain formation [ChIP-Seq, 2]

(Submitter supplied) Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL17021 GPL19057
26 Samples
Download data: BW
Series
Accession:
GSE103258
ID:
200103258
19.

Capturing the onset of PRC2-mediated repressive domain formation

(Submitter supplied) Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin. This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL19057 GPL17021
107 Samples
Download data: BEDGRAPH, BW
Series
Accession:
GSE94431
ID:
200094431
20.

Capturing the onset of PRC2-mediated repressive domain formation (RNA-Seq)

(Submitter supplied) Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17021
13 Samples
Download data: XLS
Series
Accession:
GSE94430
ID:
200094430
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