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Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance [T47D]

ABSTRACT: Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance [T47D]

PROVIDER: PRJNA490630 | ENA |

REPOSITORIES: ENA

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Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance [T47D]

Project description:To establish a data-driven learning model of the temporal dynamics and 3D chromatin reorganization, we conducted tethered chromatin conformation (TCC) sequencing to examine 3D structure dynamics in estradiol (E2)-induced breast cancer T47D cells and Tamoxifen resistant breast cancer T47D cells.

2019-04-09 | GSE119890 | GEO

Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance

Project description:Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance

| PRJNA428600 | ENA

Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance

Project description:To establish a data-driven learning model of the temporal dynamics and 3D chromatin reorganization, we conducted tethered chromatin conformation (TCC) sequencing to examine 3D structure dynamics in estradiol (E2)-induced breast cancer MCF7 cells and Tamoxifen resistant breast cancer MCF7 cells.

2019-04-09 | GSE108787 | GEO

Temporal dynamic reorganization of 3D chromatin architecture in hormone-induced breast cancer and endocrine resistance.

Project description: Not available

| S-EPMC6447566 | biostudies-literature

Time-resolved DNA methylation profiling of endocrine resistance in the T47D luminal A breast cancer cell line

Project description:Endocrine therapy is the most used treatment for hormone receptor positive breast cancers. Despite the clear benefit of endocrine therapy for patients with ER+ breast cancer, resistance to treatment is a critical clinical issue affecting a large number of patients. While many studies have shown that genetics is an important factor in therapy resistance, recent publications have also reported that epigenetics might play a major role in the acquisition of resistance to endocrine therapies. This role is exploited both at the DNA methylation level, with activation of oncogenes and silencing of tumor suppressor genes, and at the histone modification level, with changes in chromatin accessibility. DNA methylation exerts its role in resistance both by targeting the ER itself, by inducing promoter methylation, and genome wide, by changing the methylation levels of estrogen response elements. To better understand resistance acquisition in an in vitro setting, researchers developed cellular models of endocrine therapy resistance. The prevalent strategy to identify mechanisms of resistance development and novel targets involved in the process has been to study differences between resistant and sensitive cells. Here, we performed time-resolved DNA methylation profiling of development of resistance to tamoxifen treatment and to estrogen deprivation in the T47D luminal A breast cancer cell line with the aim to identify novel drivers.

2020-07-17 | GSE154626 | GEO

RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

Project description:RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

| PRJNA807652 | ENA

T47D shNT versus T47D shRON

Project description:T47D shNT versus T47D shRON

| PRJNA682172 | ENA

RNA-seq analysis of hormone receptor positive breast cancer cell line T47D with 24h hormone treatment

Project description:T47D cells treated with hormones 24h

2022-03-31 | GSE196876 | GEO

T47D cell line transfected with various ESR1 fusion genes (or with estrogen treatment), vs. YFP transfection alone

Project description:Gene expression profiling of the downstream transcriptional changes induced by ESR1 fusion genes observed in human breast tumors resistant to hormone therapy Experimental T47D cells stably expressing ESR1 fusion genes (or T47D cells treated with estradiol) vs. T47D cells expressing YFP

2015-06-12 | E-GEOD-69774 | biostudies-arrayexpress

Gene expression in human breast cancer T47D cells associated with expression of PTH-AS, a lncRNA downstream of parathyroid hormone

Project description:To comprehensively analyze the effect of PTH-AS on gene expression, microarray analysis was performed using human breast cancer T47D cells expressing PTH-AS. The gene expression levels of full-length PTH-AS expressing T47D cells (T47D-PA6) and vector control (T47D-VC1) or incomplete PTH-AS expressing T47D cells (T47D-PA5) were compared. As a result, 1453 genes were differentially expressed in his T47D-PA6 compared to T47D-VC1. Except for genes whose expression was altered in T47D-PA5 cells expressing incomplete PTH-AS, PTH-AS expression in T47D cells upregulated 914 genes and downregulated 600 genes. Many of the altered genes have been classified as immune-related biological processes. Particularly striking was the significant upregulation of JAK-STAT pathway-related genes, including the interferon-related DNA damage resistance signature (IRDS) that promotes cancer.

2022-05-21 | GSE176467 | GEO

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