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Promoter methylation data: OHT/ICI-sensitive vs. -resistant cell lines

ABSTRACT: MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation. Two comparisons: OHT-resistant vs. wild type, and ICI-resistant vs. wild type. OHT: 4-hydroxytamoxifen ICI: fulvestrant ((ICI 182780) This submission represents the methylation component of the study.

ORGANISM(S): Homo sapiens

SUBMITTER: Jaesik Jeong

PROVIDER: E-GEOD-25519 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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An empirical Bayes model for gene expression and methylation profiles in antiestrogen resistant breast cancer.

Jeong Jaesik J Li Lang L Liu Yunlong Y Nephew Kenneth P KP Huang Tim Hui-Ming TH Shen Changyu C

BMC medical genomics 20101125

<h4>Background</h4>The nuclear transcription factor estrogen receptor alpha (ER-alpha) is the target of several antiestrogen therapeutic agents for breast cancer. However, many ER-alpha positive patients do not respond to these treatments from the beginning, or stop responding after being treated for a period of time. Because of the association of gene transcription alteration and drug resistance and the emerging evidence on the role of DNA methylation on transcription regulation, understanding ...[more]

PMID: 21108837

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Promoter methylation data: OHT/ICI-sensitive vs. -resistant cell lines

Project description:MCF7 breast cancer cell lines: drug-resistant (OHT and ICI) cell lines vs. drug-sensitive (wild type) cell lines. Assessment of association between gene expression and methylation.

2011-10-05 | GSE25519 | GEO

The expression patterns of 17b-estradiol responsive genes in wt MCF7, OHT resistant MCF7 and ICI resistant MCF7

Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Keywords: 17b-estradiol responsive genes, OHT resistance, Fulvestrand resistance

2007-09-14 | GSE5840 | GEO

Transcription profiling of human wild type MCF7, OHT resistant MCF7 and ICI resistant MCF7 17b-estradiol responsive genes

Project description:Compare the expression pattern of 17b-estradiol responsive genes in parent, OHT-resistant and ICI-resistant breast cancer cells. Experiment Overall Design: Data for 4 replicate experiments performed with biologically independent samples. Experiment Overall Design: KN01M001v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01H002v0 DMSO (control) wt MCF7 -> GSM136148 Experiment Overall Design: KN01H003v0 DMSO (control) wt MCF7 -> GSM136150 Experiment Overall Design: KN01H004v0 DMSO (control) wt MCF7 -> GSM136152 Experiment Overall Design: KN01M005v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136153 Experiment Overall Design: KN01H006v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136154 Experiment Overall Design: KN01H007v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136155 Experiment Overall Design: KN01H008v0 17b-estradiol (10nM 4h) wt MCF7 -> GSM136156

2008-06-14 | E-GEOD-5840 | biostudies-arrayexpress

Homo sapiens

Project description:Promoter methylation data: OHT/ICI-sensitive vs. -resistant cell lines

| PRJNA133775 | ENA

ER-dependent gene expression in LY2 cell line

Project description:ER-dependent gene expression was investigated in the LY2 endocrine resistant cell line by treatment with ICI 182780. Cells were steroid depleted for 3 days prior to treatment with ICI for 6 hours. Four biological replicates were processed and analysed.

2014-09-18 | E-MTAB-1870 | biostudies-arrayexpress

Mouse iPS cells-derived 3D-retinas: Vehicle control- vs. 4-hydroxytamoxifen (4-OHT)-treated 3D-retinas w/o supplements

Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control with 4-OHT-treated w/o supplements. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRÎ²), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of protective effects of representative ophthalmic supplements for treating the photoreceptor degeneration. 4-OHT w/o supplements-induced gene expression in the 3D-retinas was measured at DD 25 when the photoreceptor cells started to be degenerated. Four-condition experiment, vehicle control- vs. 5 ÂµM 4-OHT- vs. 5 ÂµM 4-OHT with 400 ÂµM vitamin E- vs. 5 ÂµM 4-OHT with 200 nM lutein-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1replicate.

2016-07-05 | E-GEOD-83984 | biostudies-arrayexpress

Project description:Genetic analyses of ICI-sensitive vs. ICI-resistant RenCa cells

| PRJNA1199538 | ENA

Mouse iPS cells-derived 3D-retinas: Vehicle control- vs. 4-hydroxytamoxifen (4-OHT)-treated 3D-retinas

Project description:Transcriptional profiling of 3D-retinas differentiated from mouse iPS cells comparing vehicle control- with 4-OHT-treated. 4-OHT is an inverse agonist of estrogen-related receptor beta (ERRÎ²), a rod-enriched transcription factor responsible for maintenance of rod photoreceptor cells and the treatment induces photoreceptor specific cell death in the 3D-retinas. Goal was to understand the mechanism of 4-OHT-induced degeneration of photoreceptor cells in the 3D-retinas. 4-OHT-induced gene expression in the 3D-retinas was measured at DD 26 when the photoreceptor cells were degenerated. Two-condition experiment, vehicle control- vs. 5 ÂµM 4-OHT-treated 3D-retinas. Biological replicates: each sample has 24 3D-retinas and 1 replicate.

2016-07-05 | E-GEOD-83985 | biostudies-arrayexpress

Transcription profiling of human MCF-7 breast cancer cells treated with E2, ICI 182,789 (ICI), Raloxifene (Ral), and/or trans-hydroxytamoxifen (TOT)

Project description:MCF-7 breast cancer cells were treated with E2, ICI 182,789 (ICI), Raloxifene (Ral), and/or trans-hydroxytamoxifen (TOT) for 8 or 48 h. Duplicate samples are labeled set A or set B.

2007-09-27 | E-GEOD-848 | biostudies-arrayexpress

ICI-SJS/TEN mediated by macrophage-derived CXCL10 and abated by TNF blockade

Project description:Immune checkpoint inhibitors (ICI) represent new anticancer agents and have been used worldwide. However, ICI can potentially induce life-threatening severe cutaneous adverse reaction (SCAR), such as Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), hindering continuous ICI therapy. We examined 6 cohorts within 25 ICI-induced SJS/TEN patients and conducted single-cell RNA sequencing (scRNA-seq) analysis, which revealed overexpression of macrophage-derived CXCL10 that recruited CXCR3+ cytotoxic T lymphocytes (CTL) in blister cells from ICI-SJS/TEN skin lesions. ScRNA expression profiles and ex vivo blocking studies further identified TNF signaling as the key pathway responsible for macrophage-derived CXCL10 and CTL activation. Based on the trajectory analysis, ICI-activated T cells from whole blood are proposed to serve as the initial cells involved in inflammation, that lead to monocytes differentiating into macrophages and increasing their susceptibility to migrate to the lesion sites. Compared with systemic corticosteroids treatment, ICI-induced SJS/TEN patients treated with biologic TNF blockade showed a significantly rapid recovery and no recurrence of SCAR with continuous ICI therapy. Our findings identified that macrophage-eliciting CTL contribute the pathogenesis of ICI-induced epidermal necrolysis and provide the therapeutic targets for the management and prevention of SCAR induced by ICI therapy.

2024-08-26 | GSE273720 | GEO

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