Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
Project description:The hallmark of human cancer is heterogeneity, mirroring the complexity of genetic and epigenetic alterations acquired during oncogenesis. We extracted RNA of 34 cultured human ovarian carcinoma cell lines and performed expression microarrays so that cultured cell lines can represent in vivo human tumors. 34 ovarian carcinoma cell lines expression data.
Project description:Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines
Project description:The hallmark of human cancer is heterogeneity, mirroring the complexity of genetic and epigenetic alterations acquired during oncogenesis. We extracted DNA of 14 cultured human ovarian carcinoma cell lines subjected to pooled shRNA screen using TRC 1.0 library, and performed DNAseq. 14 ovarian carcinoma cell lines DNAseq data.
Project description:Based on a time-course study of cisplatin response in ovarian cancer cells with/without suppression of annexin A11 expression using whole genome oligonucleotide microarrays, we identified a set of differentially expressed genes associated with annexin A11 expression and patterns of gene expressions in response to cisplatin exposure. Keywords: human ovarian cancer cell lines 2008 cells (one ovarian cancer cell line) were transfected with ANXA11_RNAi or control_RNAi for 2 days and then treated with 10 µM cisplatin (Sigma) for 0, 8, 16, 24 hours. Total RNA of 8 samples were prepared for gene expression profiling using the Agilent 44K whole genome oligonucleotide microarrays.
Project description:The hallmark of human cancer is heterogeneity, mirroring the complexity of genetic and epigenetic alterations acquired during oncogenesis. We extracted RNA of 34 cultured human ovarian carcinoma cell lines and performed expression microarrays so that cultured cell lines can represent in vivo human tumors.
Project description:To determine the signaling networks that are dysregulated in platinum-resistant ovarian cancer, gene expression data were obtained from, and compared between, the ovarian cancer cell line, A2780, and its cisplatin-resistant derivative, A2780cis. Gene expression data from a cisplatin-sensitive ovarian cancer cell line (A2780) were collected and compared to gene expression data from a cisplatin-resistant cell line (A2780cis). 6 independent experiments were completed for both the sensitive and resistant cell lines.
Project description:We treated 8 human ovarian cancer cell lines with cisplatin in treatment/recovery cycles to induce in-vitro resistance to the drug. Microarrays measured gene expression at baseline and after each dose schedule (after recovery).
Project description:Background. Genome-wide expression changes are associated with development of chemoresistance in patients with ovarian cancer (OVCA); the BCL2 antagonist of cell death (BAD) apoptosis pathway may play a role in clinical outcome. Methods. We analyzed specimens and/or genomic data from 1,406 patients and 116 cancer cell lines. Genome-wide expression changes and cisplatin-resistance were evaluated in OVCA cell lines subjected to a total of 144 (cisplatin)-treatment/recovery cycles. Pathway analysis was performed on genes associated with increasing cisplatin-resistance. BAD protein phosphorylation was studied in patient samples and cell lines, and small interfering RNAs (siRNA) used to explore the pathway as a therapeutic target. We evaluated the influence of BAD-pathway expression on chemosensitivity and/or clinical outcome using genomic data from 60 human cancer cell lines and ovarian, breast, colon, and brain cancers from 1,258 patients. Results. The BAD pathway was associated with evolution of OVCA cell line cisplatin-resistance (P<0.001) and resistance of 7 human cancer cell types to 8 cytotoxic agents (P<0.05). OVCA chemoresistance was associated with BAD protein phosphorylation, and targeted siRNA modulation produced corresponding changes in chemosensitivity. Expression of a 47-gene BAD-pathway signature was associated with survival of 1,258 patients with ovarian, breast, colon, and brain cancer. The OVCA BAD-pathway signature survival advantage was independent of surgical cytoreductive status. Conclusions. The BAD apoptosis pathway influences the sensitivity of human cancers to a variety of chemotherapies, likely via modulation of BAD-phosphorylation. The pathway has clinical relevance as a potential biomarker of therapeutic response, patient survival, and as a promising therapeutic target. Twenty-eight (28) advanced-stage serous epithelial ovarian cancers were resected at the time of primary surgery from patients who would receive platinum-based therapy. The tumors were arrayed on Affymetrix HG-U133A GeneChips. The samples were analyzed with respect to the BAD pathway for correlation to overall survival and cisplatin response.