Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 & GAR15-13 RNA-seq]

ABSTRACT: The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 & GAR15-13 RNA-seq]

PROVIDER: PRJNA509776 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8315110.fastq.gz	Fastqsanger.gz
	SRR8315120.fastq.gz	Fastqsanger.gz
	SRR8315101.fastq.gz	Fastqsanger.gz
	SRR8315111.fastq.gz	Fastqsanger.gz
	SRR8315121.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 ChIP-seq]

Project description:The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 ChIP-seq]

| PRJNA533223 | ENA

The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 ChIP-seq]

Project description:The role of the androgen receptor (AR) in estrogen receptor alpha (ER) positive breast cancer is controversial, constraining implementation of AR-directed therapies. Using a diverse, clinically relevant panel of cell-line and patient-derived models, we demonstrate that AR activation, not suppression, exerts potent anti-tumor activity in multiple disease contexts, including resistance to standard-of-care ER and CDK4/6 inhibitors. Importantly, AR agonists combined with standard-of-care agents enhanced therapeutic responses. Mechanistically, agonist activation of AR altered the genomic distribution of ER and essential co-activators (p300, SRC-3), resulting in repression of ER-regulated cell cycle genes and up-regulation of AR target genes, including known tumor suppressors. A gene signature of AR activity positively predicted disease survival in multiple clinical ER+ breast cancer cohorts. These findings provide unambiguous evidence that AR has a tumor suppressor role in ER+ breast cancer and support AR agonism as the optimal AR-directed treatment strategy, revealing a rational therapeutic opportunity.

2021-01-18 | GSE129930 | GEO

The Androgen Receptor is a Tumor Suppressor in Estrogen Receptor Positive Breast Cancer [PDX model HCI-005 & GAR15-13 RNA-seq]

2021-01-18 | GSE123763 | GEO

HCI-PDX Trial Center for Breast Cancer Therapy

Project description:HCI-PDX Trial Center for Breast Cancer Therapy

| PRJNA741291 | ENA

HCI-PDX Trial Center for Breast Cancer Therapy

Project description:HCI-PDX Trial Center for Breast Cancer Therapy

| PRJNA741292 | ENA

Characterization of a novel hormone-responsive endometrial cancer cell line: HCI-EC-23 [RNA-seq]

Project description:Most endometrial cancers are driven by excess estrogen signaling and express the hormone receptor estrogen receptor alpha (ER). Evaluation of the estrogen response in endometrial cancer cells has been limited by the availability of hormonally responsive in vitro models, with one cell line, Ishikawa, being used in most studies. Here, we describe a novel, adherent endometrioid endometrial cancer (EEC) cell line model, HCI-EC-23. We show that HCI-EC-23 retains ER expression and that ER functionally responds to 17b-estradiol (E2) induction over a range of passages. We also demonstrate that this cell line retains paradoxical activation of ER by tamoxifen, which is also observed in Ishikawa and is consistent with clinical data. The mutational landscape shows that HCI-EC-23 is mutated at many of the commonly altered genes in EEC, has relatively few copy-number alterations, and is microsatellite instable high (MSI-high). In vitro proliferation of HCI-EC-23 is modestly enhanced by E2 but is strongly reduced upon combination E2 and progesterone (P4) treatment. HCI-EC-23 exhibit strong E2 dependence for tumor growth in vivo and tumor size is reduced by combination E2 + P4 treatment. Molecular characterization of E2 induction in HCI-EC-23 revealed hundreds of estrogen-responsive genes that significantly overlapped with those regulated in Ishikawa. Analysis of ER genome binding identified similar patterns in HCI-EC-23 and Ishikawa, although ER exhibited more bound sites in Ishikawa. This study demonstrates that HCI-EC-23 is estrogen-responsive and can be used to study the hormonal aspects of endometrial cancer.

2022-08-02 | GSE210123 | GEO

Characterization of a novel hormone-responsive endometrial cancer cell line: HCI-EC-23 [ChIP-seq]

2022-08-02 | GSE210122 | GEO

Androgen receptor is a back-door inhibitor of Androgen Receptor is a Backdoor Inhibitor of Wildtype and Mutant Estrogen Receptors in Refractory Hormone Receptor-Positive Breast Cancers

Project description:HCI-13 patient-derived xenograft was treated with vehicle or a tissue-selective androgen receptor modulator (SARM), enobosarm. RNA was extracted from the tumors and microarray was performed. Objective: The objective of the study is to determine the effect of an androgen receptor (AR) agonist or a selective AR modulator (SARM) on hormone receptor-positive breast cancer growth in preclinical models and to determine the underlying mechanism of action.

2019-07-31 | GSE126318 | GEO

Reversible LSD1 Inhibition with HCI-2509 induces the p53 gene expression signature in high-risk neuroblastoma cells

Project description:Lysine-Specific Demethylase 1 (LSD1) over-expression correlates with poorly differentiated neuroblastoma and predicts poor outcome despite multimodal therapy. We have studied the efficacy of reversible and specific LSD1 inhibition with HCI-2509 in neuroblastoma cell lines and particularly the effect of HCI-2509 on the transcriptomic profile in MYCN amplified NGP cells. Cell survival assays show that HCI-2509 is cytotoxic to poorly differentiated neuroblastoma cell lines in low micromole or lower doses. Transcriptional profiling of NGP cells treated with HCI-2509 shows a significant effect on p53, cell cycle, MYCN and hypoxia pathway gene sets. HCI-2509 results in increased histone methyl marks and p53 levels along with cell cycle arrest in the G2/M phase and inhibition of colony formation of NGP cells. Our findings indicate that LSD1 inhibition with HCI-2509 has a multi-target effect in MYCN amplified high-risk neuroblastoma cells.

2019-01-01 | GSE104526 | GEO

Expression data of LUAD cell line PC9 treated with 2 uM HCI-2509 for 48 hours

Project description:The epigenetic regulator LSD1 is overepxpressed in lung adenocarcinoma (LUAD). HCI-2509 a LSD1 inhibitor leads to growth arrest in in vitro tumor models. To identify the underlying molecular mechanims behind LSD1 overexpression, we examined the gene expression patterns using microarray in the LUAD cell line PC9 after HCI-2509 treatment

2018-07-27 | GSE117702 | 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