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Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE116919 | GEO | 2019/07/09

REPOSITORIES: GEO

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Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)

Project description:Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) alone and in combination for 72 hours

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Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (ChIPseq)

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Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination

Project description:Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination

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Response and resistance to BET bromodomain inhibitors in triple-negative breast cancer.

Project description: Not available

| S-EPMC4854653 | biostudies-literature

Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (ChIPseq)

Project description:Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (ChIPseq)

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Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)

Project description:Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)

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Response and resistance to BET bromodomain inhibitors in triple negative breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-07 | E-GEOD-63584 | biostudies-arrayexpress

Synthetic Lethal and Resistance Interactions with BET Bromodomain Inhibitors in Triple-Negative Breast Cancer.

Project description: Not available

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Response and resistance to BET bromodomain inhibitors in triple negative breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-01-07 | GSE63584 | GEO

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

Project description: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. After engendering acquired resistance to BET inhibition in previously sensitive TNBCs, we utilized integrative approaches to identify a unique mechanism of epigenomic resistance to this epigenetic therapy. Resistant cells remain dependent on BRD4, confirmed by RNA interference. However, TNBC cells adapt to BET bromodomain inhibition by re-recruitment of unmutated BRD4 to super-enhancers, now in a bromodomain-independent manner. Proteomic studies of resistant TNBC identify hyper-phosphorylation of BRD4 and strong association with MED1. Together, these studies provide a rationale for BET inhibition in TNBC and argue for combination strategies to anticipate clinical drug resistance. RNA-Seq in parental and JQ1 resistant triple negative breast cancer (TNBC) in response to DMSO or JQ1 treatment over time

2016-01-07 | E-GEOD-63582 | biostudies-arrayexpress

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