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Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)

ABSTRACT: Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)

OTHER RELATED OMICS DATASETS IN: GSE14551GSE14550GSE14552

PROVIDER: PRJNA114391 | ENA |

REPOSITORIES: ENA

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Gene expression profiling of tumor stroma of MCF7 breast cancer xenografts overexpressing podoplanin (mouse array)

Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify potential molecular mediators of podoplanin-induced effects in the murine tumor stroma we compared transcriptional profiles of podoplanin-overexpressing and control tumors using mouse microarrays. Keywords: comparative transcriptional profiling

2010-05-25 | GSE14551 | GEO

Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)

Project description:Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)

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Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin (human array)

Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify molecular mediators of podoplanin-induced effects we compared transcriptional profiles of podoplanin-overexpressing and control tumors. Keywords: comparative transcriptional profiling

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Expression data from MCF7 wt and MCF7/HER2-18 xenografts

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Gene expression profiling of MCF7 breast cancer xenografts overexpressing podoplanin

Project description:This SuperSeries is composed of the SubSeries listed below.

2010-05-25 | GSE14552 | GEO

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

RNA-Seq of MCF7 intraductal xenografts hormonally treated

Project description:RNA-Seq of MCF7 intraductal xenografts hormonally treated

| PRJNA793248 | ENA

Transcription profiling of mouse MCF7 wt 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. 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-8140 | biostudies-arrayexpress

RNA-Seq of CTRL and PGR overexpressing MCF7 intraductal xenografts

Project description:Using a large variety of methods we demostrate that PGR can be a driver of tumor proliferation even in absence of extensive E2. In this specific experiment we overexpress PGR in MCF7 cells intraductally xenografted into the ductal tree of a mouse mammary gland, which provides post-menopausal levels of E2. Despite these conditions the cells thrive and with the PGR overexpression the growth rate is double the control cells. PGR overexpressing cells exhibit consistently more invasive and metastatic properties.

2022-04-05 | GSE192808 | GEO

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