Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression associated with endocrine therapy resistance in estrogen receptor-positive breast cancer

ABSTRACT: Gene expression analysis to study early-stage estrogen receptor-positive breast cancer patient associated with endocrine therapy resistance.

ORGANISM(S): Homo sapiens

PROVIDER: GSE285299 | GEO | 2024/12/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression associated with endocrine therapy resistance in estrogen receptor-positive breast cancer

Project description:Gene expression associated with endocrine therapy resistance in estrogen receptor-positive breast cancer

| PRJNA1202185 | ENA

Metabolomic Rewiring in Endocrine Therapy-Resistant Estrogen Receptor Positive Breast Cancer

Project description:Metabolomic Rewiring in Endocrine Therapy-Resistant Estrogen Receptor Positive Breast Cancer

| PRJNA1003494 | ENA

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer [ChIP-Seq]

Project description:The transcriptional activity of the TEAD4 trascription factor requires co-activators. In this study we found that the expression of the TEAD coactivator VGLL1 is repressed in estrogen receptor positive breast cancer but upon resistance to endocrine threapies VGLL1 is expressed to high levels. To elucidate the importance of the coactivator VGLL1 in breast cancer cells resistant to endocrine therapies and to identify the VGLL1 target genes, we performed ChIP-seq for VGLL1 in MCF7 breast cancer cells resistant to fulvestrant (FULVR) and ChiP-seq for TEAD4 in FULVR cells and the isogenic MCF7 cells.

2023-12-05 | GSE216525 | GEO

Gene expression associated with endocrine therapy resistance in estrogen receptor-positive breast cancer.

Project description:Despite endocrine therapy (ET), approximately 20-40% of Stage I-III estrogen receptor-positive breast cancer (ER + BC) patients experience recurrence. Recurrence while on ET is indicative of ET resistance. This study aimed to identify differentially expressed genes (DEGs) associated with recurrence during ET (ET resistance) and to explore gene expression differences across PAM50 molecular subtypes. Eighty tumor specimens from 79 patients treated at the City of Hope Comprehensive Cancer Center (2012-2016) were analyzed using NanoString technology. Fourteen patients (17.7%) experienced recurrence over a median follow-up of 68 months (range 35-104 months). Key upregulated DEGs in the recurrence group included EZH2 (log2 fold change[log2FC]: 0.67, p = 0.0017), WNT11 (log2FC: 1.08, p = 0.0088), ITGB6 (log2FC: 0.80, p = 0.0312), and TOP2A (log2FC: 0.79, p = 0.0381). Downregulated DEGs included SNAI2 (log2FC: - 0.63, p = 0.0055), ITPR1 (log2FC: - 0.75, p = 0.0083), CD10 (log2FC: - 0.70, p = 0.0092), PTEN (log2FC: - 0.29, p = 0.0163), VRD (log2FC: - 0.46, p = 0.0184), and WNT5A (log2FC: - 0.76, p = 0.0272). EZH2 and TOP2A were positively correlated with proliferation scores, while WNT11 and ITGB6 emerged as potential biomarkers independently associated with recurrence. These findings suggest novel biomarker candidates that could help overcome ET resistance, reduce recurrence, and improve outcomes in ER + BC.

| S-EPMC11871144 | biostudies-literature

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

Project description:The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that breast cancer cells undergo genome-wide reprogramming of their chromatin landscape, defined by epigenomic maps and chromatin openness, as they acquire resistance to endocrine therapy. This reveals a role for the Notch pathway while excluding classical ERa signaling. In agreement, blocking Notch signaling, using gamma-secretase inhibitors, or targeting its downstream gene PBX1 abrogates growth of endocrine therapy-resistant breast cancer cells. Moreover Notch signaling through PBX1 directs a transcriptional program predictive of tumor outcome and endocrine therapy response. Comparing histone modifications (H3K4me2 and H3K36me3), chromatin openness (FAIRE) and PBX1 binding between endocrine therapy sensitive MCF7 and resistant MCF7-LTED cells.

2013-05-01 | E-GEOD-37323 | biostudies-arrayexpress

Phosphoproteomics measurement of clonal endocrine therapy sensitive and resistant breast cancer populations

Project description:Around two thirds of breast tumors are characterized by the expression of estrogen receptor α and are therapeutically treated by blocking estrogen signaling. First line endocrine therapeutics are Tamoxifen which displaces estrogen form its receptor preventing receptor activation and aromatase inhibitors which prevent the formation of estrogen and thereby hormone-deprive the tumors. Therapy resistance remains a major clinical problem, especially for patients with late-stage diagnoses. Tumor heterogeneity may promote therapy resistance either through the selection of pre-existing rare clones or by providing a repertoire of cells that may develop resistance over time. In order to study endocrine therapy resistance on a clonal level, we have developed barcoded (allowing the tracking of single cells) endocrine therapy sensitive and resistant breast cancer cell lines. From these complex cell pools, multiple single cells characterized by a specific barcode were isolated and grown out. We then subjected the clones to phosphoproteomics measurement by Mass spectrometry. Based on their phosphorylation pattern, the kinase activity profiles of endocrine therapy resistant clones were determined to identify differentially activated kinases with implications in therapy resistance.

2024-01-26 | PXD040478 | Pride

VGLL1 drives therapy resistance in estrogen receptor positive breast cancer

Project description:VGLL1 drives therapy resistance in estrogen receptor positive breast cancer

| PRJNA894162 | ENA

Genome-wide reprogramming of the chromatin landscape underlies endocrine therapy resistance in breast cancer

2013-05-01 | GSE37323 | GEO

FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response

Project description:This SuperSeries is composed of the following subset Series: GSE25314: FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part I) GSE25315: FoxA1 is a critical determinant of Estrogen Receptor function and endocrine response (part II) Refer to individual Series

2010-11-17 | E-GEOD-25316 | biostudies-arrayexpress

Estrogen-induced lncRNA, LINC02568, promotes estrogen receptor-positive breast cancer development and drug resistance through both in trans- and in cis-mechanisms

Project description:Estrogen and estrogen receptor (ER) signaling play critical roles in the development of ER-positive breast cancer, and endocrine therapy is the frontline treatment for ER-positive breast cancer patients. However, the primary and acquired resistance to endocrine therapy including tamoxifen and fulvestrant remains as the major challenge in the clinic. Here, we identified an estrogen-induced lncRNA, LINC02568, through transcriptomic analysis, which is highly expressed in ER-positive breast cancer. LINC02568 is functional important in ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as endocrine therapy resistance. Mechanically, we demonstrated that LINC02568 regulates, in trans, estrogen/ERα-induced gene transcriptional activation by sponging miR-1233-5p to stabilize ESR1 mRNA in the cytoplasm. Meanwhile, LINC02568 contributes to tumor-specific pH homeostasis in breast cancer cells by regulating CA12 in cis in the nucleus. The dual functions of LINC02568 together contribute to breast cancer cell growth and tumorigenesis as well as endocrine therapy resistance. Antisense oligonucleotides (ASO) targeting LINC02568 significantly inhibits ER-positive breast cancer cell growth in vitro and tumorigenesis in vivo as well as resensitize tamoxifen-resistant cells to tamoxifen. Furthermore, combination treatment with ASO targeting LINC02568 and tamoxifen exhibits synergistic effect on tumor growth. Taken together, our findings revealed dual mechanisms of LINC02568 in regulating ERα signaling and pH homeostasis in ER-positive breast cancer, and indicated that targeting LINC02568 might represent a potential therapeutic avenue in clinic.

2023-09-13 | GSE217190 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data