Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA123257 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE15372: Expression data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines. GSE15373: Promoter CpG island methylation data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines. Refer to individual Series
2009-04-17 | E-GEOD-15709 | biostudies-arrayexpress
Project description:Promoter CpG island methylation data from A2780 (cisplatin-sensitive) and Round5 A2780 (cisplatin-resistant) cell lines.
| PRJNA122939 | ENA
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.
2011-11-05 | E-GEOD-33482 | biostudies-arrayexpress
Project description:The aim of this experiment was to evaluate the changes in gene expression in response to hypoxia and/or cisplatin in an ovarian cancer cell line model. A2780 (cisplatin-sensitive) and A2780cis (cisplatin-resistant) cell lines were treated with cisplatin in normoxia or hypoxia (0.5% O2) for 72 hours. RNA was extracted from three independent biological replicates for each condition: A2780 (normoxia, untreated); A2780 (hypoxia, untreated); A2780 (normoxia, cisplatin); A2780cis (hypoxia, cisplatin), A2780cis (normoxia, untreated); A2780cis (hypoxia, untreated); A2780cis (normoxia, cisplatin); A2780cis (hypoxia, cisplatin) and interrogated on Affymetrix Human Gene ST 1.0 arrays.
2016-01-15 | E-MTAB-3645 | biostudies-arrayexpress
Project description:Cisplatin and carboplatin are the primary first-line therapies for the treatment of ovarian cancer. However, resistance to these platinum-based drugs occurs in the large majority of initially responsive tumors, subsequently resulting in a poor long-term prognosis. To model the onset of drug resistance, we measured gene expression alterations associated with cisplatin resistance. We treated clonally derived, drug-sensitive A2780 epithelial ovarian cancer cells with increasing concentrations of cisplatin. After 5 cycles of drug selection, the isogenic drug-sensitive (parental A2780) and -resistant (Round5 A2780) cell lines were subjected to mRNA expression microarray analyses.
2009-04-17 | E-GEOD-15372 | biostudies-arrayexpress
Project description:Multiple DNA methylation changes have been associated with the acquisition of drug resistance; however it remains uncertain how many of these changes may represent critical DNA methylation drivers of chemoresistance. Using genome-wide DNA methylation profiling across 27,578 CpG sites on Illumina HumanMethylation27 bead array we identified loci at 4092 genes becoming hypermethylated in the chemoresistant A2780/cp70 ovarian tumour cell line compared to the parental sensitive A2780 line. Hypermethylation at CpG islands (CGI) is often associated with transcriptional silencing, however only 245 of these hypermethylated genes become down-regulated in A2780/cp70 as measured by microarray expression profiling. Treatment with the demethylating agent Decitabine induces re-sensitisation to cisplatin and resulted in re-expression of 41 of the down-regulated genes in cisplatin-resistant cells at the time point when re-sensitisation occurs. 13 of the 41 genes were consistently hypermethylated in two further independent cisplatin-resistant A2780 cell derivatives. Nine out of the 13 genes (ARHGDIB, ARMCX2, COL1A, FLNA, FLNC, MEST, MLH1, NTS, PSMB9) acquired methylation at CpG sites in ovarian tumours at relapse following chemotherapy or chemoresistant cell lines derived at the time of patient relapse. Furthermore, 5/13 candidate genes acquired methylation in drug-resistant in vivo-derived ovarian cancer sustaining (side population) cells. Therefore, this small set of genes are potential key drivers of chemoresistance and should be further evaluated as predictive biomarkers, both to existing chemotherapies, but also to epigenetic therapies used to modulate drug resistance. Array-based methylation profiling was performed using the Infinium HumanMethylation27 BeadChip in two cisplatin sensitive cell lines and three cisplatin resistant cell lines derived in vitro, four pairs of cisplatin sensitive and resistant cell lines derived in vivo, 7 pairs of tumour tissues obtained from patients before chemotherapy and at disease relapse, 2 pairs of IGROV1 SP and NSP cells. The reproducibility of the Infinium HumanMethylation27 BeadChips was evaluated using biological and technical replicates of matched chemosensitive/chemoresistant ovarian cancer cell lines PEO1/PEO4. Differential methylation cutoff was estimated from two biological replicates by bootstrap resampling.
2011-12-20 | E-GEOD-28647 | biostudies-arrayexpress
Project description:A2780 and cisplatin resistant cell line A2780-DR RNA-seq
| PRJNA304713 | ENA
Project description:We conducted a comprehensive genomic characterization of the cisplatin sensitive A2780 ovarian cancer cell line compared to A2780cis, its resistant derivative. The data includes eXcision Repair-sequencing (XR-seq) to map cisplatin repair,RNA-Seq to characterize gene expression and ATAC-Seq to detect changes in chromatin accessibility.
2021-06-07 | GSE173201 | GEO
Project description:Differences in gene expression in A2780C20 vs. A2780 and A2780 treated with temsirolimus at 24-hr and 48-hr. The A2780 are human ovarian carcinoma cellls were purchased to the European Collection of Cell Cultures (ECACC). The A2780CP20 are cisplatin resisatnt cells derived of the A2780 cells. A2780CP20 cells were generated by Dr. Robert Ozols (J. Natl. Cancer Inst. 84, 264-267 (1992) by treatment of A2780 cells with incresing concentrations of cisplatin. The goal of this study is to determine whether the cisplatin and temsirolimus resistance are co-regulated. The objectives of this study are to identify additional genes differentially expressed in cisplatin sensitive and cisplatin resistant ovarain cancer cells and the changes in gene expreession upon temsirolimus treatment of A2780 cells.
2013-10-25 | GSE51683 | GEO