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Links from GEO DataSets

Items: 20

1.

Therapeutic Targeting of BET Bromodomain Proteins in Castration-Resistant Prostate Cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL15433 GPL4133
83 Samples
Download data: BW, TXT
Series
Accession:
GSE55064
ID:
200055064
2.

Therapeutic Targeting of BET Bromodomain Proteins in Castration-Resistant Prostate Cancer (microarray)

(Submitter supplied) Men who develop metastatic castration-resistant prostate cancer (CRPC) invariably succumb to the disease. The development and progression to CRPC following androgen ablation therapy is predominantly driven by unregulated androgen receptor (AR) signaling1-3. Despite the success of recently approved therapies targeting AR signaling such as abiraterone4-6 and second generation anti-androgens MDV3100 (enzalutamide)7,8, durable responses are limited, presumably due to acquired resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL4133
48 Samples
Download data: TXT
Series
Accession:
GSE55063
ID:
200055063
3.

Therapeutic Targeting of BET Bromodomain Proteins in Castration-Resistant Prostate Cancer (ChIP-Seq)

(Submitter supplied) Men who develop metastatic castration-resistant prostate cancer (CRPC) invariably succumb to the disease. The development and progression to CRPC following androgen ablation therapy is predominantly driven by unregulated androgen receptor (AR) signaling1-3. Despite the success of recently approved therapies targeting AR signaling such as abiraterone4-6 and second generation anti-androgens MDV3100 (enzalutamide)7,8, durable responses are limited, presumably due to acquired resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL15433
35 Samples
Download data: BW
Series
Accession:
GSE55062
ID:
200055062
4.

Contribution of BET proteins to androgen (DHT)-stimulated gene expression program

(Submitter supplied) Competitive inhibitors of acetyl-lysine binding to the bromodomains of the BET (bromodomain and extra terminal) family are being developed for the treatment of solid and heme malignancies. BET family member BRD4 function at enhancers/super-enhancers has been shown to sustain signal-dependent or pathogenic gene expression programs. Here we tested the hypothesis that the transcription factor drivers of castration-resistant prostate cancer (CRPC) clinical progression, including the Androgen Receptor (AR), are critically dependent on BRD4 and thus represent a sensitive solid tumor indication for the BET inhibitor ABBV-075. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
8 Samples
Download data: CEL
Series
Accession:
GSE86245
ID:
200086245
5.

Identification of HOXB13 target genes responsive to BET inhibitors

(Submitter supplied) We identified BRD4 as an epigenetic regulator of the prostate lineage specific gene HOXB13 during progression of the disease from an androgen dependent to an androgen independent state.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
9 Samples
Download data: TXT
6.

Gene Expression Analysis of metastatic CRPC cell line C4-2B treated with the dual BET-kinase inhibitor MA4-022-1

(Submitter supplied) We identified BRD4 as an epigenetic regulator of the prostate lineage specific gene HOXB13 during progression of the disease from an androgen dependent to an androgen independent state.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18460
2 Samples
Download data: TXT
7.

BET Bromodomain Inhibition Blocks the Function of a Critical AR-Independent Master Regulator Network in Lethal Prostate Cancer

(Submitter supplied) BET bromodomain inhibitors are known to block prostate cancer cell survival through suppression of c-Myc and androgen receptor (AR) function. However, little is known about other transcriptional modulators whose function is blocked by these drugs and the anti-tumor activity of BET bromodomain inhibition in AR-independent castration-resistant prostate cancers (CRPC), whose frequency may be increasing. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
34 Samples
Download data: BED, TXT
8.

Transcriptome analysis of VCaP xenografts resistant to dual therapy with abiraterone and enzalutamide

(Submitter supplied) We report RNA sequencing data on serial biopsies of prostate cancer VCaP xenografts as the tumors pass from androgen-sensitivity (Pre-Cx), to castration resistance (CRPC, castration resistant prostate cancer), onto resistance to dual therapy with abiraterone plus enzalutamide (AER). From comparison of these RNAseq data sets, we were able to determine differentially expressed genes between the AER/CRPC and Pre-Cx states that could mediate resistance to androgen deprivation therapies.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: TXT
9.

Profiles of prostate cancer cell lines

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Other; Expression profiling by high throughput sequencing
Platform:
GPL11154
32 Samples
Download data: TXT
Series
Accession:
GSE87153
ID:
200087153
10.

Cellular androgen content influences enzalutamide agonism of F877L mutant androgen receptor

(Submitter supplied) Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) – the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
30 Samples
Download data: TXT
11.

Response and resistance to BET bromodomain inhibitors in triple negative 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
Platforms:
GPL11154 GPL18573
65 Samples
Download data: WIG
Series
Accession:
GSE63584
ID:
200063584
12.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [RNA-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL18573 GPL11154
28 Samples
Download data: TXT
13.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [ChIP-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
35 Samples
Download data: WIG
Series
Accession:
GSE63581
ID:
200063581
14.

Response and resistance to BET bromodomain inhibitors in triple negative breast cancer [Chem-Seq]

(Submitter supplied) Triple negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease for which there is no targeted therapy. Here we report the preferential and high sensitivity of TNBCs to BET bromodomain inhibitors such as JQ1 manifested by cell cycle arrest in early G1, apoptosis, and induction of markers of luminal epithelial differentiation in vitro and in vivo. The sensitivity of TNBC and other tumor types to BET inhibition establishes a rationale for clinical investigation, and a motivation to understand mechanisms of resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: WIG
Series
Accession:
GSE63284
ID:
200063284
15.

Targeting the EWS/ETS transcriptional program by BET bromodomain inhibition in Ewing sarcoma

(Submitter supplied) Ewing sarcomas (ES) are highly malignant, osteolytic bone or soft tissue tumors, which are characterized by early metastasis into lung and bone. Genetically, ES are defined by balanced chromosomal EWS/ETS translocations, which give rise to chimeric proteins (EWS-ETS) that generate an oncogenic transcriptional program associated with altered epigenetic marks throughout the genome. By use of an inhibitor (JQ1) blocking BET bromodomain binding proteins (BRDs) we strikingly observed a strong down-regulation of the predominant EWS-ETS protein EWS/FLI1 in a dose dependent manner. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE72673
ID:
200072673
16.

Determining the impact of the Bromodomain and extra-terminal inhibitor JQ1 on the GATA2 cistrome in castrate-resistant prostate cancer

(Submitter supplied) To determine the impact of the Bromodomain and extra-terminal (BET) inhibitor JQ1 on the GATA2 cistrome in castrate-resistant prostate cancer we performed GATA2 ChIP-seq in the presence and absence of JQ1 and assessed differential binding upon JQ1 treatment for 24 hours. We first determined the GATA2 cistrome using our GATA2 ChIP-seq data. Overlapping this with previously published ChIP-seq data for the BET family of proteins (Asangani et al., 2014), we identified a substantial proportion of GATA2 genomic binding sites which are co-occupied by a BET protein. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
8 Samples
Download data: NARROWPEAK
Series
Accession:
GSE125236
ID:
200125236
17.

LSD1 inhibition disrupts super-enhancer activities in CRPC

(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:
GPL16791 GPL30173 GPL18573
58 Samples
Download data: MTX, TSV
Series
Accession:
GSE209889
ID:
200209889
18.

LSD1 inhibition disrupts super-enhancer activities in CRPC [scRNA-seq]

(Submitter supplied) Our studies revealed a novel oncogenic function of LSD1 in driving PCa progression by activating MYC signaling and mediating CRPC SEs activities, cotargeting LSD1 and BRD4 achieved significant synergistic effects in repressing CRPC tumor growth
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
2 Samples
Download data: MTX, TSV
Series
Accession:
GSE209888
ID:
200209888
19.

LSD1 inhibition disrupts super-enhancer activities in CRPC [RNA-seq]

(Submitter supplied) Our studies revealed a novel oncogenic function of LSD1 in driving PCa progression by activating MYC signaling and mediating CRPC SEs activities, cotargeting LSD1 and BRD4 achieved significant synergistic effects in repressing CRPC tumor growth
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL30173 GPL16791
54 Samples
Download data: TXT
Series
Accession:
GSE209887
ID:
200209887
20.

LSD1 inhibition disrupts super-enhancer activities in CRPC [ChIP-seq]

(Submitter supplied) Our studies revealed a novel oncogenic function of LSD1 in driving PCa progression by activating MYC signaling and mediating CRPC SEs activities, cotargeting LSD1 and BRD4 achieved significant synergistic effects in repressing CRPC tumor growth
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL16791
2 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE209886
ID:
200209886
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