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Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the EGFR-specific inhibitor gefitinib for 45 hours

ABSTRACT: Results of blocking EGFR kinase activity in MCF-10A cells by treatment with gefitinib and measuring gene expression as a function of time provides information as to what genes are regulated by EGFR in these nontransformed breast epithelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23135 | GEO | 2010/08/24

SECONDARY ACCESSION(S): PRJNA133237

REPOSITORIES: GEO

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Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the EGFR-specific inhibitor gefitinib for 45 hours

Project description:Results of blocking EGFR kinase activity in MCF-10A cells by treatment with gefitinib and measuring gene expression as a function of time provides information as to what genes are regulated by EGFR in these nontransformed breast epithelial cells. MCF-10A cells were treated with the EGFR-specific small molecule kinase inhibitor gefitinib for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2010-08-24 | E-GEOD-23135 | biostudies-arrayexpress

Genome-wide analysis of time-dependent gene expression in MCF-10HER-2 cells treated with the EGFR-specific inhibitor gefitinib for 45 hours

2010-08-24 | GSE23136 | GEO

Genome-wide analysis of time-dependent gene expression in MCF-10HER-2 cells treated with the EGFR-specific inhibitor gefitinib for 45 hours

Project description:Results of blocking activated EGFR/HER-2 heterodimer signaling in MCF-10HER-2 cells by treatment with gefitinib and measuring gene expression as a function of time provides information as to what genes are regulated by EGFR/HER-2 signaling in these breast epithelial cells that are transduced to overexpress the HER-2 oncogene and express transformed phenotypes. MCF-10HER-2 cells were treated with the EGFR-specific small molecule kinase inhibitor gefitinib for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2010-08-24 | E-GEOD-23136 | biostudies-arrayexpress

Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the HER-2-specific inhibitor CP724,714 for 45 hours

2011-03-18 | GSE23138 | GEO

Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the HER-2-specific inhibitor CP724,714 for 45 hours

Project description:Results of blocking HER-2 kinase activity in MCF-10A cells by treatment with CP724,714 and measuring gene expression as a function of time provides information as to what genes are regulated by HER-2 in these nontransformed breast epithelial cells. MCF-10A cells were treated with the HER-2-specific small molecule kinase inhibitor CP724,714 for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2011-03-18 | E-GEOD-23138 | biostudies-arrayexpress

Gefitinib treatment in human EGFR-driven-Gefitinib resistant tumoral cell line

Project description:In order to analyze the molecular effect of the combination of Notch inhibitors and EGFR inhibitors on resistance to TKI, we performed RNA-seq gene expression profiling of PC9 resistant to Gefitinib cells treated with different combinations.

2021-07-01 | GSE117846 | GEO

Gefitinib treatment in human EGFR-driven-Gefitinib resistant tumoral cell line

Project description:Gefitinib treatment in human EGFR-driven-Gefitinib resistant tumoral cell line

| PRJNA483409 | ENA

Transcriptomic analysis of gefitinib-resistant EGFR-mutant NSCLC cells

Project description:We have employed a transcriptomic approach to find a molecular target that could compensate for the loss of EGFR signaling in NSCLC cell lines with acquired resistance to gefitinib with an EMT phenotype.

2019-12-31 | GSE123066 | GEO

Transcription profiling of Human Endometrial Cancer Cells treated with EGF or gefitinib to investigate gene regulation of EGFR Isoforms.

Project description:Microarrays were used to analyze differential gene expression and to help determine the efficacy of Iressa (gefitinib), a tyrosine kinase inhibitor, on endometrial cancer cells. Type I Ishikawa H and type II Hec50co endometrial carcinoma cells both express EGFR and sEGFR, but differ markedly in their responsiveness to the EGFR inhibitor gefitinib. This difference is paralleled by differences in the expression of sEGFR and EGFR, as well as in their transcriptional response following treatment with either EGFor gefitinib. The small cluster of differently regulated genes reported here in these type I vs. type II endometrial cancer-derived cell lines may identify candidate biomarkers useful for predicting sensitivity to EGFR blockade. Type I (Ishikawa H cells) and type II (Hec50co) derived endometrial carcinomas, were dosed with either EGF(epidermal growth factor) or Iressa (gefitinib) for 12 or 24 hours and gene expression was examined.

2010-03-23 | E-GEOD-20854 | biostudies-arrayexpress

JUN-Mediated downregulation of EGFR signaling is associated with resistance to gefitinib in EGFR-mutant NSCLC cell lines [ChIP-seq]

Project description:The Epidermal Growth Factor Receptor (EGFR) regulates a diverse set of biological processes including cell growth, proliferation, and differentiation. Deregulation of the EGFR pathway has been implicated in a variety of human diseases including cancer. Gefitinib and erlotinib are tyrosine kinase inhibitors (TKIs) that have demonstrated clinical benefit for patients with Non-small cell lung cancer (NSCLC) and EGFR activating mutations. However, patients invariably acquire resistance to TKI treatment through a number of mechanisms. We utilized in vitro models of NSCLC with EGFR activating mutations and derived three isogenic cell lines with acquired resistance to gefitinib. We next studied genomewide mRNA expression in resistance and wild type cells and their effect in the reprogramming of pathways in lung cancer cell line models..

2017-06-02 | GSE95590 | GEO

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