Ena-DATASET-BCCA-10-01-2019-07:50:58:269-1167 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001004553 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:10X genomics chromium single-cell RNA-sequencing of (i) patient derived triple negative breast cancer xenograft (ii) primary tumour and ascites ovarian cancer cell lines at tumour recurrence.
| EGAD00001004552 | EGA
Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2. Three biological replicates (MASE2 tumours grown in SCID mice, see growth protocol) were analyzed for both conditions of addition of E2 or placebo.
2014-01-20 | E-GEOD-45271 | biostudies-arrayexpress
Project description:Exogenous 17β-estradiol (E2) accelerates the progression of ovarian cancer in the transgenic tgCAG-LS-TAg mouse model of the disease. We hypothesized that E2 has direct effects on ovarian cancer cells and this study was designed to determine the molecular mechanisms by which E2 accelerates ovarian tumour progression. Mouse ovarian cancer ascites (MASE2) cell lines were derived from tgCAG-LS-TAg mice. Following intraperitoneal engraftment of MASE2 into SCID mice, exogenous E2 significantly decreased the survival time and increased the tumour burden. Microarray analysis performed on cells derived from mouse ovarian cancer ascites (MASE2) treated with and without E2 indicated that E2 treatment caused the upregulation and downregulation of genes involved in cell differentiation, proliferation and migration. In particular, Greb1 that has been also identified as a hormone-responsive gene in breast cances, was upregulated in mouse tumour cells treated with E2.
2014-01-20 | GSE45271 | GEO
Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Illumina HT-12 v4 arrays were performed according to the manufacturer's directions on total RNA extracted from i) tumour cells purified from ovarian tumour ascites, and ii) established cell lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
2016-08-11 | E-GEOD-71524 | biostudies-arrayexpress
Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Illumina HumanMethylation450 arrays were performed according to the manufacturer's directions on DNA extracted from i) tumour cells purified from ovarian tumour ascites, and ii) established cell lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
2016-08-11 | E-GEOD-71523 | biostudies-arrayexpress
Project description:This study aimed to generate a new panel of comprehensively, genomically characterized high-grade serous ovarian carcinoma (HGSOC) cell line and xenograft models. Multidimensional genomic data were generated and compared between cell lines/xenografts and the tumours they were derived from, indicating the cell lines/xenografts are highly similar to their patient-matched tumours. Cell line/xenograft data were also compared to TCGA ovarian tumours to show the cell lines are good models of clinical HGSOC. Affymetrix SNP 6 arrays were performed according to the manufacturer's instructions on genomic DNA extracted from i) tumour cells purified from ovarian tumour ascites, ii) established cell lines, iii) patient derived xenografts, and iv) lymphoblast lines. Evaluation of the similarity in copy number/methylation/gene expression/mutational profiles of cell lines/tumours/xenografts was performed.
2016-08-11 | E-GEOD-71522 | biostudies-arrayexpress
Project description:Primary tumor recurrence occurs commonly after surgical resection of lung squamous cell carcinoma (SCC). The aim of this study was to identify genes involved in recurrence in lung squamous cell carcinoma patients. Array comparative genomic hybridization (aCGH) was performed on DNA extracted from tumour tissue from 62 patients with primary lung squamous cell carcinomas. aCGH data was analysed to identify genes affected by copy number alterations that may be involved in SCC recurrence. Candidate genes were then selected for technical validation based on differential copy number between recurrence and non-recurrence SCC tumour samples. Genes technically validated advanced to tests of biological replication by qPCR using an independent test set of 72 primary lung SCC tumour samples. 18q22.3 loss was identified by aCGH as significantly associated with recurrence (p=0.038). Although aCGH copy number loss associated with recurrence was found for seven genes within 18q22.3, only SOCS6 copy number loss was both technically replicated by qPCR and biologically validated in the test set. DNA copy number profiling using 44K element array comparative genomic hybridization microarrays of 62 primary lung squamous cell carcinomas.
2011-12-25 | E-GEOD-32058 | biostudies-arrayexpress
Project description:Ascites or solid tumour samples from patients with ovarian cancer were collected and grown in culture as ex vivo models of purified tumour cells. RNA-seq was performed on these models to establish gene expression profiles, which allow identification of genes that are differentially expressed between patients with differing tumour intrinsic properties. These samples have been interrogated for the presence of a gene expression signature indicative of sensitivity to an inhibitor of poly(ADP-ribose) glycohydrolase (PARG). These samples are processed in the same manner as previous studies: “E-MTAB-7223 - RNA-seq of human ex vivo ovarian cancer models with matched stromal cells” and “E-MTAB-10801 - RNA-seq of human ex vivo ovarian cancer models with matched stromal cells - part II” with no stromal counterparts included in this current sequencing batch.
2021-10-10 | E-MTAB-11000 | biostudies-arrayexpress
Project description:Primary tumor recurrence occurs commonly after surgical resection of lung squamous cell carcinoma (SCC). The aim of this study was to identify genes involved in recurrence in lung squamous cell carcinoma patients. Array comparative genomic hybridization (aCGH) was performed on DNA extracted from tumour tissue from 62 patients with primary lung squamous cell carcinomas. aCGH data was analysed to identify genes affected by copy number alterations that may be involved in SCC recurrence. Candidate genes were then selected for technical validation based on differential copy number between recurrence and non-recurrence SCC tumour samples. Genes technically validated advanced to tests of biological replication by qPCR using an independent test set of 72 primary lung SCC tumour samples. 18q22.3 loss was identified by aCGH as significantly associated with recurrence (p=0.038). Although aCGH copy number loss associated with recurrence was found for seven genes within 18q22.3, only SOCS6 copy number loss was both technically replicated by qPCR and biologically validated in the test set.
2011-12-25 | GSE32058 | GEO