GEO DataSets

(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

(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

(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

(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

(Submitter supplied) Illumina array was employed to analyze the genes whose expression are altered when ARID1A gene is downregulated by shRNA in normal ovarian surface epithelial cells OSE4 and IOSE80pc. This leads to discovery of p53-regulated genes such as p21 and SMAD3.

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4826

Platform:

GPL10558

4 Samples

Download data: TXT

Analysis of OSE4 and IOSE80pc ovarian surface epithelial cells depleted for ARID1A, which encodes large nuclear protein p270. ARID1A depletion enhances OSE4 and IOSE80pc proliferation. OSE4 cells become highly tumorigenic upon ARID1A depletion. Results suggest a tumor-suppressor role for ARID1A.

Organism:

Homo sapiens

Type:

Expression profiling by array, transformed count, 2 cell line, 2 protocol sets

Platform:

GPL10558

Series:

GSE37684

4 Samples

Download data

(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

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

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17692

8 Samples

Download data: CEL

(Submitter supplied) To define the gene profile altered by EZH2 and H3K27me3 in response to IFNg, we performed several microarrays in primary ovarian cancer cells transfected with shEZH2 or treated with GSK126. We found that 155 and 124 genes were altered by shEZH2 and GSK126 treatment, respectively, and 20 genes were increased or decreased by both shEZH2 and GSK126 treatment.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17692

4 Samples

Download data: CEL

(Submitter supplied) To define the gene profile altered by EZH2 and H3K27me3 in response to IFNg, we performed several microarrays in primary ovarian cancer cells transfected with shEZH2 or treated with GSK126. We found that 155 and 124 genes were altered by shEZH2 and GSK126 treatment, respectively, and 20 genes were increased or decreased by both shEZH2 and GSK126 treatment.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17692

4 Samples

Download data: CEL

(Submitter supplied) CNV profiling of tumors obtained from our Chaos3 mouse model for spontaneous breast cancer. The goal of this experiment was to determine copy number variations that were specific to MTs derived from this mouse model, when comapared to non-MTs.

Organism:

Mus musculus

Type:

Genome variation profiling by genome tiling array

Platform:

GPL10448

15 Samples

Download data: TXT

(Submitter supplied) The goal of this study was to identify important genetic pathways that are altered in mammary tumor cells upon over-expression of the tumor suppressor gene Arid1a. The results of this experiment revealed that Arid1a helps regulate key cell-cycle checkpoint and growth regulatory pathways, either directly or indirectly. This helped explain in part the significant decrease in cell proliferation and tumor growth phenotypes observed both in vitro and in vivo, when comparing the same samples analyzed here by RNA-seq (untransduced replicates vs. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL17021

4 Samples

Download data: DIFF, TXT

(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

(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:

GPL20301

8 Samples

Download data: TXT

(Submitter supplied) mTORC1 is a conserved central controller of cell growth, which is commonly activated in hepatocellular carcinoma (HCC), driving liver tumorigenesis. In addition to its established cytoplasmic functions, mTORC1 is found in the nucleus where it regulates transcription by all three major RNA polymerases. However, precisely how mTORC1 controls gene expression remains poorly understood. Herein we show that mTORC1 interacts with the BAF SWI/SNF complex and regulates genome-wide chromatin remodeling through ARID1A. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20301

4 Samples

Download data: TXT

(Submitter supplied) mTORC1 is a conserved central controller of cell growth, which is commonly activated in hepatocellular carcinoma (HCC), driving liver tumorigenesis. In addition to its established cytoplasmic functions, mTORC1 is found in the nucleus where it regulates transcription by all three major RNA polymerases. However, precisely how mTORC1 controls gene expression remains poorly understood. Herein we show that mTORC1 interacts with the BAF SWI/SNF complex and regulates genome-wide chromatin remodeling through ARID1A. more...

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platform:

GPL20301

4 Samples

Download data: TXT

(Submitter supplied) There is a long-established connection between epigenetic reprogramming and the local function of the spliceosome. Recently the oncogenic potential of this connection has also been recognized. Recent work has demonstrated that EWS-FLI1 recruits the BRG1/BRM-associated factor (BAF) complex, however, the specific BAF subunits that interact with EWS-FLI1 and the role of the BAF complex in oncogenesis remains unknown. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10332

12 Samples

Download data: TXT

(Submitter supplied) We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers with targeted DNA methylation-independent alterations in nucleosome occupancy.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing; Methylation profiling by high throughput sequencing

Platform:

GPL11154

2 Samples

Download data: BED, BW

(Submitter supplied) We show that knocking down ARID1A in an immortalized endometriosis cell line leads to phenotypic changes in vitro. Additionally, we find strong increases in the active H3K27ac mark in promoter regions but decrease of H3K27ac at potential enhancers.

Organism:

Homo sapiens

Type:

Genome binding/occupancy profiling by high throughput sequencing

Platforms:

GPL11154 GPL18573

18 Samples

Download data: TXT