U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

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
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
7.

ARID1A-deficient Bladder Cancer is Dependent on PI3K Signaling, and can be Targeted via EZH2 and/or PI3K Pharmacologic Inhibition: Therapeutic Implications

(Submitter supplied) ARID1A-mutant bladder cancer is dependent on PI3K signaling and is sensitive to EZH2 and/or PI3K inhibition. Clinical trials in molecularly selected patients should be considered.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL21697
12 Samples
Download data: BED, BIGWIG
Series
Accession:
GSE203033
ID:
200203033
8.

Transcriptomic profiling for differential gene expression in ARID1A-wt and ARID1A-deficient bladder cancer cells with and without GSK126 (an EZH2 inhibitor) treatment

(Submitter supplied) Metastatic urothelial carcinoma of the bladder is generally incurable with current systemic therapies. Chromatin modifiers are frequently mutated in bladder cancer, with ARID1A inactivating mutations present in 20% of tumors. EZH2 is a histone methyltransferase that acts as an oncogene that functionally opposes ARID1A. In addition, PI3K signaling is activated in over 20% of bladder cancers. Here we show that ARID1A-mutant tumors are more sensitive to EZH2 inhibition than ARID1A-wild-type tumors. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21697
12 Samples
Download data: CSV
9.

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
10.

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:
GPL18573 GPL11154
8 Samples
Download data
Series
Accession:
GSE95645
ID:
200095645
11.

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
12.

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
13.

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
14.

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
15.

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
16.

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
17.

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
18.

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
19.

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
20.

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
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_66283250f4364867151c39dd|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center