Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Parallel-factor ER ChIP-seq of Breast Cancer PDX Material

ABSTRACT: Parallel-factor ER ChIP-seq of Breast Cancer PDX Material

PROVIDER: PRJNA434662 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6750060.fastq.gz	Fastqsanger.gz
	SRR6750061.fastq.gz	Fastqsanger.gz
	SRR6750062.fastq.gz	Fastqsanger.gz
	SRR6750063.fastq.gz	Fastqsanger.gz
	SRR6750064.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Parallel-factor ER ChIP-seq of Breast Cancer PDX Material

Project description:To demonstrate the versatility of parallel-factor ChIP-seq, we applied our method to the analysis of ER binding in five patient-derived xenograft (PDX) samples.

2018-02-21 | GSE110824 | GEO

Effects of Polybrominated Diphenyl Ether (PBDE) Mixture on estrogen receptor positive (ER+) patient-derived tumor xenograft (PDX) model

Project description:ER+ PDX (COH-SC31) were exposed to PBDE mixture for 1 weeks. RNA-sequencing analysis was performed to evalaute the gene expression changes.

2019-03-04 | GSE119587 | GEO

Copy number data from Patient-Derived tumor models (PDX) establish from bone metastases of breast cancer.

Project description:A significant proportion of patients with oestrogen receptor (ER) positive breast cancers (BC) develop resistance to endocrine treatments (ET) and relapse with metastatic disease. Bone is the most common metastatic site in ER+ patients, however bone metastases are technically challenging to biopsy and analyse. Difficulties concern both tumour tissue acquisition and techniques for analysis and RNA extractions. Patient-derived xenografts (PDX) of BC bone metastases have not been reported yet. For the first time we established PDX models from bone metastatic biopsies of patients progressing on ET and treated by vertebroplasty. PDX models were analysed at genomic level to identify new therapeutic targets associated with endocrine resistance in the metastatic setting. Identification of chromosomic alterations in bone metastasis derived PDX.

2020-06-29 | GSE149038 | GEO

RNA-seq of 7 breast PDX models treated with Fulvestrant and AZD9833/camizestrant and collected at multiple timepoints

Project description:Oral selective estrogen receptor degraders (SERDs) could become the backbone endocrine therapy (ET) for estrogen receptor-positive (ER+) breast cancer, as they achieve greater inhibition of ER-driven cancers than current ETs and overcome key resistance mechanisms. This dataset was aimed at exploring the preclinical effects of the next-generation oral SERD camizestrant (AZD9833) on 7 PDX models. Mice were treated with fulvestrant or camizestrant for 4, 24, 48, 72 hours, with at least four replicates per condition.

2023-09-11 | E-MTAB-13139 | biostudies-arrayexpress

Expression data from Patient-derived tumor models (PDX) establish from bone metastases and match human breast primary tumor.

Project description:A significant proportion of patients with oestrogen receptor (ER) positive breast cancers (BC) develop resistance to endocrine treatments (ET) and relapse with metastatic disease. Bone is the most common metastatic site in ER+ patients, however bone metastases are technically challenging to biopsy and analyse. Difficulties concern both tumour tissue acquisition and techniques for analysis and RNA extractions. Patient-derived xenografts (PDX) of BC bone metastases have not been reported yet. For the first time we established PDX models from bone metastatic biopsies of patients progressing on ET and treated by vertebroplasty. PDX models were analysed at transcriptomic level and compared to patient’s early primary tumours to identify new therapeutic targets associated with endocrine resistance in the metastatic setting. Identification of activated signalling pathways in bone metastasis by comparative transcriptomic analyses of the bone metastasis derived PDX compared to the patients' primary breast tumor.

2020-06-29 | GSE146661 | GEO

Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [PCHiC]

Project description:Here we investigate the impact of epigenetic therapy with Decitabine in endocrine-resistant ER+ breast cancer by using patient-derived xenograft (PDX) models. Decitabine treatment restrained tumour growth, inhibited cell proliferation and resulted in significant loss of DNA methylation, particularly at enhancers and repetitive elements. Systematic integration of matched in situ Hi-C / PCHi-C, EPIC, RNA-seq and ChIP–seq datasets revealed widespread differences in epigenome regulation and enhancer-promoter communication with Decitabine. We find that loss of DNA methylation with Decitabine strongly affects the open (A) and closed (B) compartment structure and TAD boundary insulation. Our study identified and focused on key DNA methylation-dependent, enhancer ER binding sites that are activated in Decitabine-treated PDX tumours, enabling direct interactions between promoters and multiple distal enhancers, inducing expression of ER target genes and pathways. Overall, we demonstrate that epigenetic therapy inhibits tumour progression through to rewiring of ER-mediated 3D chromatin interactions and transcriptome programs. Our findings suggest that targeting the 3D epigenome with epigenetic therapies represents a promising strategy for anti-cancer treatment in ER+ endocrine resistant breast cancer patients.

2021-12-12 | GSE171072 | GEO

Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [HiC]

2021-12-12 | GSE171071 | GEO

Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [RNA-seq]

2021-12-12 | GSE171073 | GEO

Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [ChIP-seq]

2021-12-12 | GSE171070 | GEO