Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA218090 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Long-term, in vitro propagation of tumor-specific endothelial cells (TEC) allows for ex vivo functional studies and gene expression profiling of clonally-derived, well-characterized subpopulations. Using a genetically-engineered mouse model (GEMM) of mammary adenocarcinoma (C3-TAg), we have optimized an isolation procedure and defined growth conditions for long-term propagation of breast TEC. Based on expression of EC-selective markers, the isolated TEC maintain their endothelial specification and phenotype in culture. Furthermore, gene expression profiling of multiple TEC subpopulations revealed striking, persistent overexpression of several candidate genes including Irx2 and Zfp503 (transcription factors), Cd166 and Cd133 (cell-surface markers), Ccl12 and neurotensin (angiocrine factors), and Gpr182 and Cnr2 (G protein-coupled receptors). Taken together, we have described an effective method for isolating and culture-expanding breast TEC from a GEMM and we have uncovered several new TEC-selective genes whose overexpression persists even after long-term in vitro culture. These results suggest that stable changes may be induced in vascular endothelial cells in the tumor microenvironment in vivo that are transmittable ex vivo. reference x sample
2014-03-21 | E-GEOD-50555 | biostudies-arrayexpress
Project description:Long-term, in vitro propagation of tumor-specific endothelial cells (TEC) allows for ex vivo functional studies and gene expression profiling of clonally-derived, well-characterized subpopulations. Using a genetically-engineered mouse model (GEMM) of mammary adenocarcinoma (C3-TAg), we have optimized an isolation procedure and defined growth conditions for long-term propagation of breast TEC. Based on expression of EC-selective markers, the isolated TEC maintain their endothelial specification and phenotype in culture. Furthermore, gene expression profiling of multiple TEC subpopulations revealed striking, persistent overexpression of several candidate genes including Irx2 and Zfp503 (transcription factors), Cd166 and Cd133 (cell-surface markers), Ccl12 and neurotensin (angiocrine factors), and Gpr182 and Cnr2 (G protein-coupled receptors). Taken together, we have described an effective method for isolating and culture-expanding breast TEC from a GEMM and we have uncovered several new TEC-selective genes whose overexpression persists even after long-term in vitro culture. These results suggest that stable changes may be induced in vascular endothelial cells in the tumor microenvironment in vivo that are transmittable ex vivo.
2014-03-21 | GSE50555 | GEO
Project description:MATERIALS AND METHODS: The genomic effects of tumor-endothelial interactions in cancer are not yet well characterized. To study this interaction in breast cancer, we set up an ex vivo coculture model with human benign and malignant breast epithelial cells with endothelial cells to determine the associated gene expression changes using DNA microarrays. RESULTS: The most prominent response to coculture was the induction of the M-phase cell cycle genes in a subset of breast cancer cocultures that were absent in cocultures with normal breast epithelial cells. In monoculture, tumor cells that contained the stem cell-like CD44(+)/CD24(-) signature had a lower expression of the M-phase cell cycle genes than the CD44(-)/CD24(+) cells, and in the CD44(+)/CD24(-) cocultures, these genes were induced. Pretreatment gene expression profiles of early-stage breast cancers allowed evaluating in vitro effects in vivo. The expression of the gene set derived from the coculture provided a basis for the segregation of the tumors into two groups. In a univariate analysis, early-stage tumors with high expression levels (n = 137) of the M-phase cell cycle genes had a significantly lower metastasis-free survival rate (P = 1.8e - 5, 50% at 10 years) and overall survival rate (P = 5e - 9, 52% at 10 years) than tumors with low expression (n = 158; metastasis-free survival, 73%; overall survival, 84%). CONCLUSIONS: Our results suggest that the interaction of endothelial cells with tumor cells that express the CD44(+)/CD24(-) signature, which indicates a low proliferative potential, might explain the unexpected and paradoxical association of the CD44(+)/CD24(-) signature with highly proliferative tumors that have an unfavorable prognosis. Computed
2010-02-17 | E-GEOD-20364 | biostudies-arrayexpress
Project description:The study aims to:
1. Achieve molecular imaging of EGFR in patients with colorectal neoplasia in vivo using confocal laser endomicroscopy.
2. Compare the results of in vivo EGFR-specific molecular imaging with CLE and ex vivo immunohistochemistry .
| 2108081 | ecrin-mdr-crc
Project description:Interactions of cancer cells with the vasculature are essential for tumor growth and likely promote metastatic progression. Endothelial cell content and lympho-vascular invasion are generally associated with tumor aggressiveness, however, these features are generally not employed in the clinic. We aimed to determine if endothelial cell gene expression signatures could be utilized to better characterize breast tumor biology, and to establish if vascular cell-derived signatures could provide information to predict tumors likely to metastasize. Here we report on the identification of a gene signature for vascular endothelial cells, and a second for cancer-activated vasculature. Both signatures independently identify subsets of aggressive breast cancers. Interestingly, the vascular content signature and a previously identified hypoxia signature both provide prognostic information beyond currently utilized clinical parameters and intrinsic subtype classifications. In these studies, we also examined the relationship that the breast cancer subtypes have with vascular gene expression profiles, and found that claudin-low tumors and cell lines express vascular gene expression profiles and displayed endothelial-like tube formation when grown in three-dimensions. These findings are directly applicable to clinical care and therapeutic treatment design as they identify highly aggressive subsets of tumors with genetic and morphologic vascular properties. reference x sample
2014-01-01 | E-GEOD-37145 | biostudies-arrayexpress
Project description:MATERIALS AND METHODS: The genomic effects of tumor-endothelial interactions in cancer are not yet well characterized. To study this interaction in breast cancer, we set up an ex vivo coculture model with human benign and malignant breast epithelial cells with endothelial cells to determine the associated gene expression changes using DNA microarrays. RESULTS: The most prominent response to coculture was the induction of the M-phase cell cycle genes in a subset of breast cancer cocultures that were absent in cocultures with normal breast epithelial cells. In monoculture, tumor cells that contained the stem cell-like CD44(+)/CD24(-) signature had a lower expression of the M-phase cell cycle genes than the CD44(-)/CD24(+) cells, and in the CD44(+)/CD24(-) cocultures, these genes were induced. Pretreatment gene expression profiles of early-stage breast cancers allowed evaluating in vitro effects in vivo. The expression of the gene set derived from the coculture provided a basis for the segregation of the tumors into two groups. In a univariate analysis, early-stage tumors with high expression levels (n = 137) of the M-phase cell cycle genes had a significantly lower metastasis-free survival rate (P = 1.8e - 5, 50% at 10 years) and overall survival rate (P = 5e - 9, 52% at 10 years) than tumors with low expression (n = 158; metastasis-free survival, 73%; overall survival, 84%). CONCLUSIONS: Our results suggest that the interaction of endothelial cells with tumor cells that express the CD44(+)/CD24(-) signature, which indicates a low proliferative potential, might explain the unexpected and paradoxical association of the CD44(+)/CD24(-) signature with highly proliferative tumors that have an unfavorable prognosis.
2010-02-18 | GSE20364 | GEO
Project description:Interactions of cancer cells with the vasculature are essential for tumor growth and likely promote metastatic progression. Endothelial cell content and lympho-vascular invasion are generally associated with tumor aggressiveness, however, these features are generally not employed in the clinic. We aimed to determine if endothelial cell gene expression signatures could be utilized to better characterize breast tumor biology, and to establish if vascular cell-derived signatures could provide information to predict tumors likely to metastasize. Here we report on the identification of a gene signature for vascular endothelial cells, and a second for cancer-activated vasculature. Both signatures independently identify subsets of aggressive breast cancers. Interestingly, the vascular content signature and a previously identified hypoxia signature both provide prognostic information beyond currently utilized clinical parameters and intrinsic subtype classifications. In these studies, we also examined the relationship that the breast cancer subtypes have with vascular gene expression profiles, and found that claudin-low tumors and cell lines express vascular gene expression profiles and displayed endothelial-like tube formation when grown in three-dimensions. These findings are directly applicable to clinical care and therapeutic treatment design as they identify highly aggressive subsets of tumors with genetic and morphologic vascular properties.
2014-01-01 | GSE37145 | GEO
Project description:RNA-Seq of ex vivo culture of circulating breast tumor cells
| PRJNA241032 | ENA
Project description:In an experimental model of tumor dormancy, heat shock protein 27 (HSP27) was up-regulated in angiogenic human breast cancer cells when compared with non-angiogenic cells. Stable down-regulation of HSP27 in angiogenic tumor cells was followed by long-term tumor dormancy in vivo and associated with reduced intra-tumoral endothelial cell proliferation, decreased secretion of VEGF and bFGF from tumor cells, and increased expression of thrombospondin-1. Phosphorylation of the transcription factor STAT3 and nuclear expression of NFκB were reduced following suppression of HSP27. In contrast, tumor cell proliferation and apoptosis were not affected. By clinical validation, high HSP27 expression was associated with markers of aggressive tumors and decreased survival in breast cancer and melanoma patients. Our present findings suggest a link between HSP27 and dormancy through tumor-vascular interactions. Targeting HSP27, a multifunctional cytoprotective protein, might offer a novel strategy in cancer treatment.
2010-02-28 | E-TABM-883 | biostudies-arrayexpress
Project description:[U-13C]-Glu SIRM study of ex vivo tissue slices in matched-pair tumor/non-tumor ex vivo tissue slices from two human patients with and without beta-glucan.
2016-03-10 | ST000367 | MetabolomicsWorkbench