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Homo sapiens

ABSTRACT: BT474 48h Lapatinib+JQ1 transcriptome response

PROVIDER: PRJNA278887 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1925361.fastq.gz	Fastqsanger.gz
	SRR1925364.fastq.gz	Fastqsanger.gz
	SRR1925394.fastq.gz	Fastqsanger.gz
	SRR1925407.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:SKBR3 48h Lapatinib+JQ1

| PRJNA278881 | ENA

Adaptive responses of the HER2+ SKBR-3 and BT474m1 cell lines to lapatinib and JQ1

Project description:SKBR-3 or BT474m1 HER2+ breast cancer cells were treated with either DMSO, 300nM lapatinib, 300nM JQ1, or lapatinib and JQ1 in combination for 48h.

2020-10-26 | GSE160018 | GEO

Human breast cancer cells: parental v.s lapatinib-resistant clone

Project description:Transcriptional profiling of human HER2-positive BT474 breast cancer cells comparing control untreated cancer cells with lapatinib-resistant clone established by chronic treatment with lapatinib

2013-10-31 | GSE51889 | GEO

BT474 and BT474-J4 microarray data

Project description:These data provide scientific information to understand the mechanism of action of lapatinib resistance in HER2-positive patients and to test the combination of HER2-targeted agents and GSK1363089 (foretinib) in the clinic by using an acquired lapatinib-resistant cell line. Cell lines (BT474, an HER2-positive and lapatinib-sensitive cell line; BT474-J4, an acquired lapatinib-resistant cell line) were treated with lapatinib alone (1uM), foretinib (GSK1363089) alone (0.1 uM), a combination of lapatinib (1 uM) and foretinib (0.1 uM), or DMSO control for 24 hours. Triplicates were performed.

2011-09-19 | E-GEOD-16179 | biostudies-arrayexpress

Homo sapiens

Project description:Lapatinib-resistant SKBR3 + JQ1 + I-BET151 for 8 days

| PRJNA278888 | ENA

Feng et al 2019 - Microarray Raw Data

Project description:In order to identify mechanisms of drug resistance to HER2-targeted therapy, we performed cDNA microarray analysis on drug naiive BT474 and drug resistant BT474 cells treated with lapatinib for 0, 10, and 20 hrs.

2020-04-14 | GSE136304 | GEO

Enhancer analysis of HER2+ cell lines SKBR-3 (ER-) and BT474m1 (ER+) in response to lapatinib and JQ1 and analysis of FOXA1 chromatin binding in SKBR-3 cells in response to lapatinib and JQ1 and impact of FOXA1 knockdown on BRD4 and MED1

Project description:SKBR-3 and BT474m1 HER2+ breast cancer cell lines were treated with lapatinib, JQ1, or lapatinib and JQ1 or (for SKBR-3) treated with siRNA pools (non-targeting control or FOXA1) prior to drug treatment before being used for ChIPseq (BRD4, MED1, H3K27Ac, or FOXA1 (for SKBR-3))

2020-11-03 | GSE160667 | GEO

Human breast cancer cells: parental v.s lapatinib-resistant clone

2013-10-31 | E-GEOD-51889 | biostudies-arrayexpress

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant âpersisterâ cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets. 3 biological replicates of BT474 persister cells, two biological replicates of BT474 parental cells

2016-07-28 | E-GEOD-84896 | biostudies-arrayexpress

Gene expression profiling of drug-tolerant persister BT474 breast cancer cells derived from lapatinib treatment

Project description:Acquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant “persister” cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets.

2016-07-28 | GSE84896 | GEO

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