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Links from GEO DataSets

Items: 20

1.
Full record GDS5816

Methyltransferase EZH2 inhibition effect on ARID1A mutated ovarian clear cell cancer cell line

Analysis of ARID1A-mutated OVISE ovarian clear cell carcinoma (OCCC) cells restored with wild-type ARID1A or treated with GSK126, an inhibitor of epigenetic regulator EZH2. Epigenetic modifier ARID1A is often mutated in OCCC. Results provide insight into the role of epigenetic mechanisms in OCCC.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 3 genotype/variation sets
Platform:
GPL10558
Series:
GSE54979
9 Samples
Download data
2.

Targeting EZH2 methyltransferase activity in ARID1A mutated cells as a synthetic lethal therapeutic strategy

(Submitter supplied) ARID1A, an epigentic modifier, is often mutated in ovarian clear cell carcinoma (OCCC). In addition, EZH2 is frequently upregulated in OCCC. Inhibtion of EZH2 with an inhibitor (GSK126) selectively inhibits ARID1A-mutated cells. This study was designed to understand changes in gene expression profiles following EZH2 inhibition or ARID1A restoration.
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS5816
Platform:
GPL10558
9 Samples
Download data: TXT
Series
Accession:
GSE54979
ID:
200054979
3.

Catalytic subunits switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells

(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 high throughput sequencing
Platform:
GPL18573
7 Samples
Download data: TXT
Series
Accession:
GSE110450
ID:
200110450
4.

Catalytic subunits switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells [RNA-seq]

(Submitter supplied) The SWI/SNF chromatin remodeling complex is altered in ~20% of human cancers. ARID1A, a component of the SWI/SNF chromatin-remodeling complex, is the most frequently mutated epigenetic regulator in human cancers. Inactivation of the SWI/SNF complex is synthetically lethal with inhibition of EZH2 activity. EZH2 inhibitors are entering clinical trials for specific tumor types with SWI/SNF mutations. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
5 Samples
Download data: TXT
Series
Accession:
GSE110449
ID:
200110449
5.

Catalytic subunits switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells [ChIP-seq]

(Submitter supplied) The SWI/SNF chromatin remodeling complex is altered in ~20% of human cancers. ARID1A, a component of the SWI/SNF chromatin-remodeling complex, is the most frequently mutated epigenetic regulator in human cancers. Inactivation of the SWI/SNF complex is synthetically lethal with inhibition of EZH2 activity. EZH2 inhibitors are entering clinical trials for specific tumor types with SWI/SNF mutations. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: TXT
Series
Accession:
GSE110448
ID:
200110448
6.

Synthetic lethality between ARID1A mutation and HDAC2 inhibition in ovarian cancer

(Submitter supplied) ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most frequently mutated epigenetic regulators in human cancers. ARID1A is mutated in over 50% ovarian clear cell carcinoma, a disease currently has no effective therapy. Here we show that ARID1A-mutated ovarian cancer cells are selectively sensitive to inhibition of HDAC2 activity. HDAC2 interacts with EZH2 in an ARID1A status dependent manner. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
3 Samples
Download data: TXT
Series
Accession:
GSE107201
ID:
200107201
7.

ARID1A-mutated ovarian cancers depend on HDAC6 activity

(Submitter supplied) ARID1A, encoding a subunit of the SWI/SNF chromatin remodeling complex, is the most mutated epigenetic regulator in human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with ARID1A mutational status remain a challenge. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated ovarian tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
5 Samples
Download data: TXT
Series
Accession:
GSE84405
ID:
200084405
8.

CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity

(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 high throughput sequencing
Platforms:
GPL11154 GPL18573
8 Samples
Download data
Series
Accession:
GSE95645
ID:
200095645
9.

CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity [RNA-Seq]

(Submitter supplied) CARM1 is an arginine methyltransferase that asymmetrically dimethylates protein substrates on arginine residues. CARM1 is often overexpressed in cancers and stimulates growth. However, clinically applicable therapeutic strategies based on CARM1 expression in cancer remains to be explored. Here we show that epithelial ovarian cancer is among the cancers with the highest CARM1 amplification rates that predicates a shorter survival. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: TXT
Series
Accession:
GSE95644
ID:
200095644
10.

CARM1-expressing ovarian cancer depends on the histone methyltransferase EZH2 activity [ChIP-Seq]

(Submitter supplied) CARM1 is an arginine methyltransferase that asymmetrically dimethylates protein substrates on arginine residues. CARM1 is often overexpressed in cancers and stimulates growth. However, clinically applicable therapeutic strategies based on CARM1 expression in cancer remains to be explored. Here we show that epithelial ovarian cancer is among the cancers with the highest CARM1 amplification rates that predicates a shorter survival. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
6 Samples
Download data: TXT
Series
Accession:
GSE95643
ID:
200095643
11.

Top2a identifies and provides epigenetic rationale for novel combination therapeutic strategies for aggressive prostate cancer

(Submitter supplied) We perform RNA-seq on matched orthotopic murine primary and metastatic prostate cancer samples to identify differential gene expressions
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
8 Samples
Download data: TXT
Series
Accession:
GSE64771
ID:
200064771
12.

Genome-wide gene expression analysis in treatment for 24 h with 40 μM APR-246 in ARID1A-WT and ARID1A-KO HCT116 cells.

(Submitter supplied) To explore the sensitivity of ARID1A-KO cells to APR-246
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13607
7 Samples
Download data: TXT
Series
Accession:
GSE122925
ID:
200122925
13.

ARID1A gene status shapes cancer immune phenotype and affects cancer immunotherapy

(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 high throughput sequencing
Platforms:
GPL20301 GPL16791
42 Samples
Download data: BW
Series
Accession:
GSE131918
ID:
200131918
14.

Intersection of ARID1A, EZH2 RNA-seq in OVCA429 cells with IFNγ treatment

(Submitter supplied) Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
16 Samples
Download data: XLSX
Series
Accession:
GSE131917
ID:
200131917
15.

RNA-seq in ARID1A WT, KO OVCA429 Cells after IFNγ treatment

(Submitter supplied) Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
18 Samples
Download data: XLSX
Series
Accession:
GSE131916
ID:
200131916
16.

ATAC-seq in ARID1A WT or KO OVCA429 Cells after interferron treatment

(Submitter supplied) Whether cancer driver mutation(s) directly drives cancer immune phenotype and immune tolerance remains a standing question. ARID1A is a core member of the polymorphic BAF chromatin remodeling complex. ARID1A mutations frequently occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A gene status on cancer immunity. We demonstrate that ARID1A mutations, limited expression, and deficiency impair interferon(IFN)-responsive gene chromatin accessibility and expression, resulting in anemic T cell tumor infiltration, weakened tumor immunity, and shortened host survival in many human cancer histologies as well as in murine cancer models, and are negatively associated with immunotherapy response. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
8 Samples
Download data: BW
Series
Accession:
GSE131915
ID:
200131915
17.

Transcriptomes change differerntly in differernt cancer cells upon EPZ-6438 treatment

(Submitter supplied) Purpose: The goals of this study are to compare NGS-derived transcriptome profiling (RNA-seq) to find out the difference between EZH2 inhibitor treatment and DMSO group in each cancer cell line, and find the relationship between transcriptomes change and drug sensivitity. Methods: mRNA profiles of cell lines were generated using Illumina PE150, then GSEA was used for cellular pathways analysis Results: The result showed 53 common oncogenic signatures were enriched in RNA-seq data. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
18 Samples
Download data: XLS
Series
Accession:
GSE119088
ID:
200119088
18.

Genome-wide Profiling of H3K27ac binding in human cancer cell lines

(Submitter supplied) Upregulation of enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) and its associated histone H3 lysine 27 (H3K27) trimethylation frequently occur in human cancer, yet both preclinical and clinical evidence suggested the very limited benefit of EZH2-targeted therapies. This study investigated the underlying mechanisms from a perspective of EZH2 inhibition-caused histone modification crosstalk. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
9 Samples
Download data: BW
Series
Accession:
GSE119086
ID:
200119086
19.

Three different in vivo models of synovial sarcoma (xenograft: Fuji; PDX: CTG-0331 and CTG-0771) treated with or without the indicated dose of the EZH2 inhibitor, tazemetostat

(Submitter supplied) The catalytic activities of covalent and ATP-dependent chromatin remodeling are central to regulating the conformational state of chromatin and the resultant transcriptional output. The enzymes that catalyze these activities are often contained within multiprotein complexes in nature. Two such multiprotein complexes, the polycomb repressive complex 2 (PRC2) methyltransferase and the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeler have been reported to act in opposition to each other during development and homeostasis. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
57 Samples
Download data: TXT
Series
Accession:
GSE83479
ID:
200083479
20.

Myc and PI3-k induced gene expression in RWPE1

(Submitter supplied) Analysis of transcriptional changes during Myc or PI3K induced oncogenic transformation in RWPE1 cells (benign prostate epithelial cell line). The aim of the present study was to identify key epigenetic gene silencing events that occur during the oncogenic transformation events, hence emphasis was placed on downregulated genes. Results provide important information on which are the tumor suppressive pathways or genes that will be epigenetically silenced by during Myc or PI3K induced oncogenic transformation.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6883
3 Samples
Download data: TXT
Series
Accession:
GSE43686
ID:
200043686
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