Affymetrix SNP array data for ovarian cancer cells OVCAR-3 and FU-OV-1
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ABSTRACT: A subset of ovarian cancer are characterized by 19q12 amplification. To perform funtional studies of this amplicon the profile has been determined by SNP analysis.
Project description:A subset of ovarian cancer are characterized by 19q12 amplification. To perform funtional studies of this amplicon the profile has been determined by SNP analysis. Affymetrix SNP arrays were performed according to the manufacturer's directions on genomic DNA extracted from ovarian cancer cell lines OVCAR-3 and FU-OV-1
Project description:Ovarian development and maintenance are poorly understood, but diseases affecting them can offer insights into their underlying mechanisms. XX-female gonadal dysgenesis (XX-GD) is a rare, genetically heterogeneous disorder characterized by underdeveloped, dysfunctional ovaries with subsequent lack of spontaneous pubertal development, primary amenorrhea, uterine hypoplasia, and hypergonadotropic hypogonadism. We used SNP arrays to perform homozygosity mapping in order to detect informative genomic regions which are homozygous and shared among affected individuals. This analysis identified genomic regions in which the mutated gene causing the XX-GD phenotype in the affected individuals may reside. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from peripheral blood samples.
Project description:Copy number profiling of 36 ovarian tumors on Affymetrix 100K SNP arrays Thirty-six ovarian tumors were profiled for copy-number alterations with the Affymetrix 100K Mapping Array. Copy number profiling of 36 ovarian tumors on Affymetrix 500K SNP arrays Sixteen ovary tumors were profiled for copy-number alterations with the high-resolution Affymetrix 500K Mapping Array.
Project description:We studied the role of miRNA-200 family members in cellular sensitivity to paclitaxel and carboplatin, using two ovarian cancer cell lines, OVCAR-3 and MES-OV, and their paclitaxel resistant variants OVCAR-3/TP and MES-OV/TP. Both resistant variants display a strong epithelial-mesenchymal transition (EMT) phenotype, with marked decreases in expression of miR-200c and miR-141 in OVCAR-3/TP, and down-regulation of all five members of the miR-200 family in MES-OV/TP. Lentiviral transfection of inhibitors of miR-200c or miR-141 in parental OVCAR-3 triggered EMT and rendered the cells resistant to paclitaxel and carboplatin. Conversely, the infection of OVCAR-3/TP cells with retroviral particles carrying the miR-200ab429 and 200c141 clusters triggered a partial mesenchymal to epithelial transition (MET). This partial MET was not sufficient to re-sensitize OVCAR-3/TP cells to paclitaxel. However, the miR-200c/miR-141 cluster transfectants became 6-8x resistant to carboplatin, an unexpected result, whereas miR-200a/miR-200b/miR-429 had no effect. Transfecting the OVCAR-3/TP GFP cells with specific miRNA mimics confirmed these data. MiR-200c and miR-141 mimics conferred resistance to carboplatin in MES-OV/TP cells, similar to OVCAR-3/TP, but sensitized MES-OV to paclitaxel. Several genes involved in balancing oxidative stress were altered in OVCAR-3/TP 200c141 cells compared to controls. The miR-200 family plays major, cell-context dependent roles in regulating EMT and sensitivity to carboplatin and paclitaxel in OVCAR-3 and MES-OV cells.
Project description:allele call files from analysis of NCI60 cell line DNA on 100K SNP arrays. Keywords = NCI60, SNP array, cancer cell line Keywords: other
Project description:Cyclin E1 (CCNE1) is amplified in various tumor types including high-grade serous ovarian cancer where it is associated with poor clinical outcome. We have demonstrate that suppression of the Cyclin E1 partner kinase, CDK2, induces apoptosis in a CCNE1 amplicon-dependent manner. Little is known of mechanisms of resistance to CDK inhibitors. We therefore generated OVCAR-3 sublines with reduced sensitivity to CDK2 inhibitors and profiled by SNP copy number microarrays.
Project description:HCC827 cells were exposed in vitro to the irreversible EGFR inhibitor PF00299804 and resistant clones were isolated. These resistant clones (HCC827 PFR) contained an amplification of the MET gene and the growth of the HCC827 PFR cells was inhibited with the combination of PF00299804 and a MET kinase inhibitor. Phenotypically, these HCC827 PFR cells were similar to our previously identified gefitinib resistant HCC827 (HCC827 GR) cells (Engelman et al. Science 2007). In order to compare global genomic changes between HCC827 GR and HCC827 PFR cells and to determine whether the MET amplicon was similar in both drug resistant cells we performed a genome wide SNP analysis.
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.