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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.

Transcriptional plasticity promotes primary and acquired resistance to BET bromodomain inhibition

(Submitter supplied) Following the discovery of BRD4 as a non-oncogene addiction target in acute myeloid leukemia (AML), BET inhibitors are being explored as promising therapeutic avenue in numerous cancers. While clinical trials have reported single-agent activity in advanced hematologic malignancies, mechanisms determining the response to BET inhibition remain poorly understood. To identify factors involved in primary and acquired BET resistance in leukemia, we performed a chromatin-focused shRNAmir screen in a sensitive MLL/AF9; NrasG12D‑driven AML model, and investigated dynamic transcriptional profiles in sensitive and resistant murine and human leukemias. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
6 related Platforms
103 Samples
Download data: BED, BW, GTF, TSV
Series
Accession:
GSE63782
ID:
200063782
6.

Spatially Constrained Tandem Bromodomain Inhibition Bolsters Sustained Repression of BRD4 Transcriptional Activity for TNBC Cell Growth

(Submitter supplied) We performed RNA-seq of MDA-MB-231 cells that were treated with MS645 or JQ1 at 50 nM and 500 nM in an effort to understand how MS645 exerts such a profound cell growth inhibition on cancer cells.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
15 Samples
Download data: TDF, TXT
7.

iBET resistance

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL6887
35 Samples
Download data: BED
Series
Accession:
GSE63683
ID:
200063683
8.

ChIP of BET proteins in iBET resistance [ChIP-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: BED, TXT
Series
Accession:
GSE63682
ID:
200063682
9.

Genome wide expression analysis of BET inhibitor resistance [RNA-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE63681
ID:
200063681
10.

Genome wide expression analysis of BET inhibitor resistance

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
14 Samples
Download data: TXT
Series
Accession:
GSE63575
ID:
200063575
11.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: H5
Series
Accession:
GSE235793
ID:
200235793
12.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [scRNA-Seq]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
8 Samples
Download data: RDATA
Series
Accession:
GSE131135
ID:
200131135
13.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platform:
GPL11154
210 Samples
Download data: BED, BW, NARROWPEAK, TXT
Series
Accession:
GSE131102
ID:
200131102
14.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [RNA-Seq]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
62 Samples
Download data: TXT
Series
Accession:
GSE131099
ID:
200131099
15.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [ChIP-Seq]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
61 Samples
Download data: BW, NARROWPEAK
Series
Accession:
GSE131097
ID:
200131097
16.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [CRISPR screen]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
44 Samples
Download data: TXT
Series
Accession:
GSE131091
ID:
200131091
17.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [Barcode_seq]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
19 Samples
Download data: TXT
Series
Accession:
GSE131030
ID:
200131030
18.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors [ATAC-Seq]

(Submitter supplied) BET bromodomain inhibitors (BBDI) are promising therapeutic agents in triple-negative breast cancer (TNBC). However, not all tumors respond and acquired resistance emerges rapidly even in the responders. Using CRISPR and small molecule inhibitor screens combined with comprehensive molecular profiling of BBDI response and resistance in TNBC cell lines, we identified numerous synthetic lethal interactions with BBDIs as well as genes that when deleted confer resistance. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
16 Samples
Download data: BED, BW
Series
Accession:
GSE131026
ID:
200131026
19.

Defining the Triple Negative Breast Cancer Kinome Response to GSK1120212 (RNA-Seq)

(Submitter supplied) LCCC1122 is a window trial in stage I-IV TNBC patients scheduled to undergo definitive surgery (either lumpectomy, mastectomy or surgical resection of oligometastatic disease). Enrolled patients will receive 1.5 -2.0 mg of the MEK1/MEK2 inhibitor GSK1120212 (trametinib; Mekinist®) orally once daily for 7 days (with treatment initiation dependent on surgical schedule) prior to their surgery, with pre- and post- treatment tissue analyzed for kinome response and resistant signatures. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
28 Samples
Download data: TXT
Series
Accession:
GSE107502
ID:
200107502
20.

Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Methylation profiling by genome tiling array; Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing; Genome variation profiling by high throughput sequencing
5 related Platforms
167 Samples
Download data: BED, CSV, IDAT, TXT, XLSX
Series
Accession:
GSE87424
ID:
200087424
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