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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

H2A.Z histone variants facilitate HDACi-dependent removal of H3.3K27M mutant protein in paediatric high-grade glioma cells

(Submitter supplied) Diffuse intrinsic pontine gliomas (DIPG) are paediatric malignant gliomas developing in the brainstem, where resection is unattainable, leaving palliative radiotherapy as the major standard of care. Patients with DIPG have dismal prognosis of 9-12 months of survival and currently there is no effective therapy. Over 80% of DIPGs harbour a mutation in histone 3 (H3.3 or H3.1) resulting in a lysine to methionine substitution (H3K27M). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL11154
47 Samples
Download data: TSV, WIG
Series
Accession:
GSE232283
ID:
200232283
5.

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
6.

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
7.

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
8.

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
9.

BAF complex maintains glioma stem cells in pediatric H3K27M-glioma

(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
Platforms:
GPL20301 GPL18573
1758 Samples
Download data: BW, CSV
Series
Accession:
GSE212786
ID:
200212786
10.

BAF complex maintains glioma stem cells in pediatric H3K27M-glioma [scRNA-seq]

(Submitter supplied) Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
1728 Samples
Download data: CSV
Series
Accession:
GSE212782
ID:
200212782
11.

BAF complex maintains glioma stem cells in pediatric H3K27M-glioma [RNA-seq]

(Submitter supplied) Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
8 Samples
Download data: CSV
Series
Accession:
GSE212718
ID:
200212718
12.

BAF complex maintains glioma stem cells in pediatric H3K27M-glioma [ChIP-seq]

(Submitter supplied) Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: BW, CSV
Series
Accession:
GSE212700
ID:
200212700
13.

BAF complex maintains glioma stem cells in pediatric H3K27M-glioma [ATAC-seq]

(Submitter supplied) Diffuse midline gliomas (DMGs) are uniformly fatal pediatric central nervous system cancers, refractory to standard of care therapeutic modalities. The primary genetic drivers are a set of recurrent amino acid substitutions in genes encoding histone H3 (H3.3 and H3.1, K27M), which are currently undruggable. These H3K27M oncohistones perturb normal chromatin architecture, resulting in an aberrant epigenetic landscape, which we interrogated here for epigenetic dependencies using a CRISPR screen in patient-derived H3K27M-glioma neurospheres. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
15 Samples
Download data: BW, TXT
Series
Accession:
GSE212679
ID:
200212679
14.

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
15.

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
16.

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
17.

Histone H3.3K27M mutation activates multiple cancer/testis antigens

(Submitter supplied) Lysine27Methionine mutations (K27M) in the histone H3 (H3.3 and H3.1) are highly prevalent in pediatric high-grade gliomas (HGG). This study found H3.3K27M caused the upregulation of multiple cancer/testis (CT) antigens, include IL13RA2 and VCX family proteins. Overexpression of VCX3A/B stimulates the expression of genes involved in immune response.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
16 Samples
Download data: TXT
Series
Accession:
GSE102886
ID:
200102886
18.

Transcriptional profiling of 2 SCCOHT PDX models and the SCCOHT cell lines BIN67 and SCCOHT1

(Submitter supplied) Transcriptional profiling of 2 SCCOHT patient-derived xenograft (PDX) models and 2 SCCOHT cell lines compared to normal ovary to investigate underlying biology of SCCOHT.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
4 Samples
Download data: TXT
Series
Accession:
GSE66434
ID:
200066434
19.

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer

(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; Other
Platforms:
GPL16791 GPL24676 GPL11154
101 Samples
Download data: BED, HIC, TXT
Series
Accession:
GSE171592
ID:
200171592
20.

Targeting SWI/SNF ATPases in enhancer-addicted prostate cancer [HiChIP-Seq]

(Submitter supplied) This study profiles chromatin accessibility, gene expresison, transcription factor binding, and three-dimensional DNA-DNA contact changes upon rapid SWI/SNF ATPase inactivation in prostate cancer cells. SWI/SNF ATPases activity was disabled using a novel PROTAC degrader compound targeting the SMARCA2, SMARCA4 and PBRM1 subunits of the SWI/SNF remodeling complex.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL24676
6 Samples
Download data: HIC
Series
Accession:
GSE171591
ID:
200171591
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