E-MTAB-10338
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-10338 | ExpressionAtlas | 2025-07-08
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-10338-analysis-methods.tsv | Tabular | |||
| E-MTAB-10338-analytics.tsv | Tabular | |||
| E-MTAB-10338-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-10338-configuration.xml | Xml | |||
| E-MTAB-10338-g2_g1-mvaPlot.png | Other |
Items per page: 5 1 - 5 of 12 |
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Project description:Microarrays were used to determine the efficacy of bevacizumab (a monoclonal antibody against the vascular endothelial growth factor and its receptors.) on endometrial cancer cells. Endometrial cancer is the most frequent gynecologic cancer in women. Long term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our work was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of antiapoptotic genes and certain proto-oncogenes. Experiment Overall Design: Human xenografts produced from endometrial cell line, grown in athymic mice, were treated in vivo with bevacizumab.
2009-11-16 | E-GEOD-18195 | biostudies-arrayexpress
Project description:Microarrays were used to determine the efficacy of bevacizumab (a monoclonal antibody against the vascular endothelial growth factor and its receptors.) on endometrial cancer cells. Endometrial cancer is the most frequent gynecologic cancer in women. Long term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our work was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of antiapoptotic genes and certain proto-oncogenes.
2009-09-22 | GSE18195 | GEO
Project description:D-glucosamine inhibits tumor growth in a xenograft mouse model, and previous studies have explored its antiproliferative mechanisms, with recent findings showing that glucosamine reduces ATP levels in cancer cells and inhibits oncogenes like IGF-1R, HIF-1α, and COX-2. However, the detailed mechanism remains unclear. To investigate further, a microarray analysis was conducted on A549 cells treated with glucosamine, identifying genes directly or indirectly affected. RNA was isolated, amplified, labeled, and hybridized to a human HT-12 expression bead chip, with data normalized using BeadStudio V3.
2025-03-18 | E-MTAB-14871 | biostudies-arrayexpress
Project description:Previous studies reported that mice living in an enriched environment (EE) showed reduced growth of melanoma, colon and breast tumors. Our study extended the potential anti-tumor effect of EE exposure to pancreatic cancer, and firstly provided evidence demonstrating that EE exposure significantly inhibits tumor growth in a syngeneic murine model of pancreatic cancer. To further investigate the mechanisms underlying the EE-induced pancreatic tumor inhibition, we analyzed the gene expression changes in pancreatic tumor xenograft using an integrative transcriptomic and proteomic approach. Our results found that EE largely decreased the expression of genes associated with mitochondrial function at transcriptional level in pancreatic tumor, suggesting mitochondrial dysfunction in tumor cells may play a critical role in EE-induced anti-tumor phenotype. Three-week-old C57BL/6 mice were randomized to live in either enriched environment or standard environment conditions. Mice from both groups were given subcutaneous injection of Panc02 murine pancreatic cancer cells (6 M-CM-^W 105 cells per mouse) and lived in their respective homes for 5 additional weeks. Pooled RNA samples extracted from Panc02 tumors (6 mice for each group) were then subjected to Agilent-014868 Whole Mouse Genome 4M-bM-^XM-^S44k Microarray analyses.
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Project description:Activating estrogen receptor alpha (ER) mutations are present in primary endometrial and metastatic breast cancers, promoting estrogen-independent activation of the receptor. Functional characterizations in breast cancer have established unique molecular and phenotypic consequences of the receptor, yet the impact of ER mutations in endometrial cancer has not been fully explored. In this study, we used CRISPR-Cas9 to model the clinically prevalent ER-Y537S mutation and compared results to ER-D538G to discover allele-specific differences between ER mutations in endometrial cancer. We found that constitutive activity of mutant ER resulted in changes in the expression of thousands of genes, stemming from combined alterations to ER binding and chromatin accessibility. The unique gene expression programs resulted in ER mutant cells developing increased cancer associated phenotypes, including migration, invasion, anchorage independent growth, and growth in vivo. To uncover potential treatment strategies, we identified ER associated proteins via Rapid Immunoprecipitation and Mass Spectrometry of Endogenous Proteins (RIME) and interrogated two candidates, CDK9 and NCOA3. Inhibition of these regulatory protein resulted in decreased growth and migration, representing potential novel treatment strategies for ER mutant endometrial cancer. Taken together, this study provides insight into ER mutant activity in endometrial cancer and identifies potential therapies for women with ER mutant endometrial cancer.
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Project description:This SuperSeries is composed of the following subset Series: GSE29435: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: cell line data GSE29436: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: patient data Refer to individual Series
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