Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of human tamoxifen-resistant MCF-7 wild-type murine xenograft tumors with E2-supplemented tumors MCF7 xenografts

ABSTRACT: In order to help determine the genes involved in resistance of breast cancer to endocrine therapy, we compared global gene expression profiles of tamoxifen-resistant MCF-7 WT xenograft tumors with E2-supplemented tumors. Experiment Overall Design: MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2) and estrogen withdrawal plus tamoxifen citrate. Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7).

ORGANISM(S): Homo sapiens

SUBMITTER: Chad Creighton

PROVIDER: E-GEOD-7327 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Tamoxifen resistance in breast tumors is driven by growth factor receptor signaling with repression of classic estrogen receptor genomic function.

Massarweh Suleiman S Osborne C Kent CK Creighton Chad J CJ Qin Lanfang L Tsimelzon Anna A Huang Shixia S Weiss Heidi H Rimawi Mothaffar M Schiff Rachel R

Cancer research 20080201 3

Not all breast cancers respond to tamoxifen, and many develop resistance despite initial benefit. We used an in vivo model of estrogen receptor (ER)-positive breast cancer (MCF-7 xenografts) to investigate mechanisms of this resistance and develop strategies to circumvent it. Epidermal growth factor receptor (EGFR) and HER2, which were barely detected in control estrogen-treated tumors, increased slightly with tamoxifen and were markedly increased when tumors became resistant. Gefitinib, which i ...[more]

PMID: 18245484

Similar Datasets

Transcription profiling of human in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively)

Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. Experiment Overall Design: MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2), continued estrogen with gefitinib (E2+G; 100mg/kg, 5 days/week), estrogen withdrawal alone (ED; by removal of the estrogen pellets), and estrogen withdrawal plus tamoxifen citrate (Tam; 500 microg/animal s.c. in peanut oil, 5 days/week), with either gefitinib (Tam+G; 100mg/kg, 5 days/week) or vehicle (1% Tween 80) administered via gavage, as well as estrogen withdrawal plus fulvestrant (ICI 182,780) in the MCF7 wt model (Fulv; 5mg/mouse s.c. once weekly), and estrogen withdrawal with gefitinib (ED+G). Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7).

2009-01-13 | E-GEOD-8139 | biostudies-arrayexpress

Transcription profiling of mouse MCF7 wt xenografts

2009-01-13 | E-GEOD-8140 | biostudies-arrayexpress

Transcription profiling of human MCF7 wt and MCF7/HER2-18 xenografts

Project description:To investigate molecular mechanisms of resistance, we used two different in vivo xenograft models of estrogen receptor-positive (ER+) breast cancer, with or without HER2 over-expression (MCF7/HER2-18 and MCF7 wt, respectively). Mice with established tumors were assigned to the following treatment groups: continued estrogen supplementation (E2), estrogen deprivation (ED), ED plus tamoxifen (Tam), all with or without the EGFR tyrosine kinase inhibitor gefinitinib (G). Another group received ED plus the antiestrogen fulvestrant (MCF7 wt only). Tumors with acquired or de novo resistance to these endocrine therapies were profiled for mRNA expression using Affymetrix Genechip arrays. This SuperSeries is composed of the following subset Series:; GSE8139: Expression data from MCF7/HER2-18 xenografts; GSE8140: Expression data from MCF7 wt xenografts Experiment Overall Design: MCF7 xenografts were established in ovariectomized five to six week-old nu/nu athymic nude mice supplemented with 0.25 mg 21 day release estrogen pellets by inoculating subcutaneously (s.c.) 5E-6 cells. When tumors reached the size of 150-200 mm3 (3-5 weeks), the animals were randomly allocated to continued estrogen (E2), continued estrogen with gefitinib (E2+G; 100mg/kg, 5 days/week), estrogen withdrawal alone (ED; by removal of the estrogen pellets), and estrogen withdrawal plus tamoxifen citrate (Tam; 500 microg/animal s.c. in peanut oil, 5 days/week), with either gefitinib (Tam+G; 100mg/kg, 5 days/week) or vehicle (1% Tween 80) administered via gavage, as well as estrogen withdrawal plus fulvestrant (ICI 182,780) in the MCF7 wt model (Fulv; 5mg/mouse s.c. once weekly), and estrogen withdrawal with gefitinib (ED+G). Tumors were harvested for molecular studies when they became resistant to treatment and reached the size of 1000 mm3 (n=7). Experiment Overall Design: Refer to individual Series

2008-12-05 | E-GEOD-8141 | biostudies-arrayexpress

Preclinical Model of ER-positive breast cancer treated with thyroid hormone with or without tamoxifen

Project description:Here, we treated a nove ER-positive PDX (UCD12) supplemented with estrogen (E2) with or without thyroid hormone (TH) and/or tamoxifen (Tam). Each treatment cohort (E2 alone, E2 + TH, E2 + Tam, E2+ TH+Tam) tumor growth over time was monitored. Tumors treated with TH continued to grow more that E2 alone. Tamoxifen blocked E2-mediated tumor growth, however in the presence of TH this was not seen. This analysis identified thyroid hormone as a potential driver of tumor progression in the context of estrogen receptor positive PDX tumor model.

2020-05-14 | GSE131276 | GEO

Radiation response in xenografts of the head and neck cancer UT14 cell line

Project description:Low passage head and neck squamous cancer cells (UT-14-SCC) were injected into the flanks of female nu/nu mice to generate xenografts. After tumors reached a size of 500mm3, they were treated with either sham RT or 15 Gy in one fraction. At different time points, days 0, 3, 10 and for controls and days 4, 7, 12, and 21 after irradiation, the tumors were harvested for global gene expression analysis and pathway analysis.

2014-09-19 | GSE61573 | GEO

Small-RNA high-throughput sequencing of head-and-neck cancer with or without human papilloma virus etiology

Project description:HPV positive head and neck cancer (HNC) are thought to have different etiology from HPV-unrelated HNC. There are indications that HPV positive HNC have better survival and that treatment options could be optimized in this set of tumours. In this study, we sought to evaluate miRNA profiles in the different groups of HNC based on cancer subsite (oral or oropharyngeal) and HPV presence (positive/negative; based on both viral DNA and RNA presence) all in comparison with normal tonsillar tissue from approximately aged subjects. From 61 enrolled patients, 22 were selected for NGS small RNA sequencing using Illumina small RNA library preparation kits and sequencing reagents on Nextseq 500 machine. Only samples with RIN >= 7 were included. manufacturers protocol was followed for library preparation. Indexing was done with indexes 1-22, and final libraries were normalizes to same amount after QBit measurement. Sequencing was done on Nextseq 500 machine and subsequent analyisis in Basespace (illumina). Raw fastq files were subsequently additionally trimmed of adapter sequences using FastQc Basespace app and differential expression evaluated with SmallRNA app. Customized plots were obtained after importing SmallRNA app calculated counts to DeSeq2 package in R and reanalysis therein.

2019-02-20 | E-MTAB-7030 | biostudies-arrayexpress

Expression data from MCF7/HER2-18 xenografts

2008-12-01 | GSE8139 | GEO

Expression data from MCF7 wt xenografts

2008-12-01 | GSE8140 | GEO

Tamoxifen treatment of MCF-7 breast cancer cells

Project description:Tamoxifen is an anti-estrogen drug used in the treatment of Estrogen Receptor (ER) positive breast cancer. Effects and side effects of tamoxifen is the sum of tamoxifen and all its metabolites. Using concentrations that mimic the clinical situation we examined effects of 4OHtam, 4OHNDtam and NDtam on global gene expression in 17beta-estradiol (E2) treated MCF-7 cells.

2014-10-24 | E-MTAB-2729 | biostudies-arrayexpress

Gene expression profiling of invasive breast cancer events from the tamoxifen prevention trial

Project description:Gene expression profiling of invasive breast cancer events from the tamoxifen prevention trial validates low estrogen receptor mRNA level as the main determinant of tamoxifen resistance in estrogen receptor positive breast cancer. In NSABP Breast Cancer Prevention Trial (BCPT), tamoxifen reduced the incidence of estrogen receptor (ER) positive tumors but not estrogen receptor negative breast cancer. More importantly, only 69% of estrogen receptor positive tumors were prevented by tamoxifen. The ER positive tumors arising in tamoxifen arm provides an ideal clinical model for acquired tamoxifen resistance. Based on data from NSABP trial B14 which showed linear prediction of the degree of benefit from adjuvant tamoxifen by the levels of ESR1 mRNA coding for ER-alpha, we hypothesized a priori that level of ESR1 mRNA would be lower in ER positive tumors arising in tamoxifen arm compared to those in placebo arm of BCPT. Keywords: Gene expression profiling analysis

2011-12-08 | GSE12665 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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