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Links from GEO DataSets

Items: 20

1.

ARID1A and the BAF complex are determinants of breast cancer treatment response [ATAC-Seq]

(Submitter supplied) Global CRISPR screens provide an unparalleled, longer-term experimental approach for the identification of essential genes in drug resistance. We used an ~18,000 gene deletion screen to discover ARID1A and other BAF complex components as the most critical factors required for response to two classes of Estrogen Receptor (ER) antagonists, namely ER degraders and Selective Estrogen Receptor Modulators (SERMs). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
24 Samples
Download data: BED
Series
Accession:
GSE134270
ID:
200134270
2.

ARID1A and the BAF complex are determinants of breast cancer treatment response

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Other; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL20301
422 Samples
Download data: BED
Series
Accession:
GSE123286
ID:
200123286
3.

ARID1A and the BAF complex are determinants of breast cancer treatment response [RNA-seq]

(Submitter supplied) Global CRISPR screens provide an unparalleled, longer-term experimental approach for the identification of essential genes in drug resistance. We used an ~18,000 gene deletion screen to discover ARID1A and other BAF complex components as the most critical factors required for response to two classes of Estrogen Receptor (ER) antagonists, namely ER degraders and Selective Estrogen Receptor Modulators (SERMs). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL20301
96 Samples
Download data: TSV
4.

ARID1A and the BAF complex are determinants of breast cancer treatment response [ChIP-seq]

(Submitter supplied) Global CRISPR screens provide an unparalleled, longer-term experimental approach for the identification of essential genes in drug resistance. We used an ~18,000 gene deletion screen to discover ARID1A and other BAF complex components as the most critical factors required for response to two classes of Estrogen Receptor (ER) antagonists, namely ER degraders and Selective Estrogen Receptor Modulators (SERMs). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL20301
267 Samples
Download data: BED
Series
Accession:
GSE123284
ID:
200123284
5.

ARID1A and the BAF complex are determinants of breast cancer treatment response [CRISPR gRNA-seq]

(Submitter supplied) Global CRISPR screens provide an unparalleled, longer-term experimental approach for the identification of essential genes in drug resistance. We used an ~18,000 gene deletion screen to discover ARID1A and other BAF complex components as the most critical factors required for response to two classes of Estrogen Receptor (ER) antagonists, namely ER degraders and Selective Estrogen Receptor Modulators (SERMs). more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL20301
35 Samples
Download data: TSV
Series
Accession:
GSE123283
ID:
200123283
6.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (RNA-seq II)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
32 Samples
Download data: TXT
7.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ChIP-seq II)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
17 Samples
Download data: BW
Series
Accession:
GSE140185
ID:
200140185
8.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer

(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:
GPL11154
103 Samples
Download data: BW
Series
Accession:
GSE124228
ID:
200124228
9.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (RNA-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: TXT
10.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ChIP-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
24 Samples
Download data: BW
Series
Accession:
GSE124225
ID:
200124225
11.

ARID1A is a critical regulator of luminal identity and therapeutic response in oestrogen receptor-positive breast cancer (ATAC-Seq)

(Submitter supplied) Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodelling complex, are the most common somatic alteration of the SWI/SNF complex across all cancers including oestrogen receptor positive (ER)+ breast cancer. We have recently reported that ARID1A inactivating mutations are present at a high frequency in advanced endocrine resistant ER+ breast cancer. In parallel, to identify mechanisms of resistance to endocrine therapy in breast cancer, we performed an epigenome CRISPR/CAS9 knockout screen that identified ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
20 Samples
Download data: BW
Series
Accession:
GSE124224
ID:
200124224
12.

Loss of ARID1A induces a stemness gene ALDH1A1 expression with histone acetylation in the malignant subtype of cholangiocarcinoma

(Submitter supplied) Genomic analyses have recently discovered the malignant subtype of human intrahepatic cholangiocarcinoma (ICC) characterized by frequent mutations of chromatin remodeling gene ARID1A, however, the biological and molecular functions still remain obscure. We here examined the clinical and biological significances of ARID1A deficiency in human ICC. Immunohistochemical analysis demonstrated that loss of ARID1A was an independent prognostic factor for overall survival of ICC patients (P = 0.023). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
4 Samples
Download data: CEL
Series
Accession:
GSE127897
ID:
200127897
13.

Differentially expressed genes following ARID1A depletion

(Submitter supplied) We konckdown ARID1A and then detected differentially expressed genes
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL21185
6 Samples
Download data: TXT
Series
Accession:
GSE116211
ID:
200116211
14.

shControl Huh7 and shARID1A Huh7 cells without or with rapamycin treatment

(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
Series
Accession:
GSE159165
ID:
200159165
15.

RNA-seq in shControl Huh7 and shARID1A Huh7 cells without or with rapamycin treatment

(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
16.

ATAC-seq in shControl Huh7 and shARID1A Huh7 cells without or with rapamycin treatment

(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
Series
Accession:
GSE159163
ID:
200159163
17.

H4K12ac is regulated by estrogen receptor-alpha and is associated with BRD4 function and inducible transcription

(Submitter supplied) Hormone-dependent gene expression requires dynamic and coordinated epigenetic changes. Estrogen receptor-positive (ER+) breast cancer is particularly dependent upon extensive chromatin remodeling and changes in histone modifications for the induction of hormone-responsive gene expression. Our previous studies established an important role of bromodomain-containing protein-4 (BRD4) in promoting estrogen-regulated transcription and proliferation of ER+ breast cancer cells. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: BIGWIG
Series
Accession:
GSE65886
ID:
200065886
18.

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
19.

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
20.

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
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