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Expression data from MCF7/HER2-18 xenografts

ABSTRACT: 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. Keywords: multiple group comparison

ORGANISM(S): Homo sapiens

PROVIDER: GSE8139 | GEO | 2008/12/01

SECONDARY ACCESSION(S): PRJNA105409

REPOSITORIES: GEO

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Expression data from MCF7 wt xenografts

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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

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Discovery of naturally occurring ESR1 mutations during acquisition of resistance to endocrine therapy in widely used estrogen receptor positive breast cancer cell lines [ChIP-Seq]

Project description:We report the first discovery of naturally occurring ESR1Y537C and ESR1Y537S mutations in MCF7 and MCF7 ESR1-positive cell-lines after acquisition of resistance to long-term-estrogen-deprivation (LTED) and subsequent resistance to fulvestrant (ICIR).

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Transcriptional profiling of antiestrogen-sensitive and -resistant MCF-7 cells

Project description:Antiestrogen-responsive (#Wt), tamoxifen-(#TamR1/8) and fulvestrant-(#FulvR6/7) cells were routinely maintained in DMEM/F12 (phenolred-free) with 1% FCS, glutamine (2mM), penicillin/streptomycin (1%) and insulin (6ng/ml). Selection was done in 1ÂµM tamoxifen or 100nM fulvestrant, respectively. For microarray studies, cells were in parallel cultured under steroid-depleted conditions: DMEM/F12 [1% charcoal-stripped, steroid-depleted FCS [CCS: (phenolred-free) with 1% FCS, glutamine (2mM), penicillin/streptomycin (1%) and insulin (6ng/ml)) for 3d and under steroid-depleted conditions treated for 1h with vehicle (DMSO), 4OHT (1ÂµM) or fulvestrant (100nM), respectively.

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Identification of human miR-22-responsive transcripts in MCF7 cells

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Identification of human miR-22-responsive transcripts in MCF7 cells

Project description:To examine the expression patterns of human miR-22-responsive transcripts in estrogen receptor alpha positive cell line MCF7, we transfected miR-22 duplex or negative control RNA duplex into MCF7 cells. Gene expression patterns were then evaluated using Affymetrix Human Genome U133 Plus 2.0 Array microarrays. Keywords: comparison of expression patterns in MCF7 cells with or without human miR-22 overexpression. Total RNA was collected from two groups MCF7-NC (MCF7 cells transfected with negative control RNA duplex) and MCF7-miR (MCF7 cells transfected with miR-22 duplex) and hybridized to Affymetrix microarrays. Each group has three repeat samples.

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