Similar Datasets
Project description:Detect the mutation in tumors with etoposide plus cisplatin treatment
2021-12-01 | GSE160239 | GEO
Project description:Parental MeWo cells sensitive to chemotherapeutic drugs Etoposide, Fotemustine, Vindesine and Cisplatin, as well as their resistant derivatives, were analyzed for expression of potential mediators of resistance using genome-wide expression profiling.
2016-03-05 | GSE78898 | 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. RNA was isolated from A2780, A2780CP20, A2780 plus temsirolimus 24-hr, and A2780 plus temsirolimus 48-hr. Labelled samples were hybridized to Affymetrix GeneChip Gene 1.0 ST Human Arrays.
2013-10-25 | E-GEOD-51683 | biostudies-arrayexpress
Project description:By using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell lines. Furthermore, we tested the sensitivity of these cell lines for cytotoxic drugs (cisplatin, etoposide, melphalan) and compared the gene-expression profile of chemotherapy-resistant and -sensitive cell lines. Staege et al., Exp Hematol 2008;36:886-896
2011-01-10 | GSE26325 | GEO
Project description:By using high-density DNA microarrays, we analyzed the gene-expression profile of Hodgkin's lymphoma cell lines. Furthermore, we tested the sensitivity of these cell lines for cytotoxic drugs (cisplatin, etoposide, melphalan) and compared the gene-expression profile of chemotherapy-resistant and -sensitive cell lines. Staege et al., Exp Hematol 2008;36:886-896 RNA was extracted from established Hodgkin's lymphoma cell lines and hybridized with Affymetrix HG_U133A microarrays.
2011-01-10 | E-GEOD-26325 | biostudies-arrayexpress
Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.
2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress
Project description:The development of chemo-resistance has dramatically limited the clinical efficiency of platinum-based therapy. Although many resistant mechanisms have been demonstrated, genetic/molecular alterations responsible for drug resistance in the majority of clinical cases has not been identified. We analyzed three pairs of testicular germ cell tumor (TGCT) cell lines using Affymetrix expression microarrays to identify differential expressed genes. Then the expression of CCND1/CyclinD1, selected from the microarray analysis, was determined in cisplatin sensitive and resistance cancer samples including TGCTs, ovarian and prostate cancers by quantitative reverse transcription PCR analysis (qRT-PCR). Finally, we determined the gene knocked-down effect of CyclinD1. Expression microarray study revealed a limited number of differentially expressed genes across all three cell lines when comparing the parental and resistant cells. Among them, CyclinD1 was the most significantly differentially expressed gene. Importantly, we found that, in clinical TGCT samples, the overall expression level of cyclinD1 is higher in resistant cases compared to those sensitive samples (9/12 in the resistant group and only 3/8 in the sensitive group). We also found that cyclinD1 expressed dozens of fold higher in the resistant than in the sensitive ovarian cancer cell lines and dramatically overexpressed in prostate cancer. We re-sensitized the resistant cells by knocking-down cyclinD1. We demonstrated that deregulation of cyclinD1 is the major cause of TGCT cisplatin resistance and it may also be commonly involved in other human cancers. Combined cyclinD1 inhibition and cisplatin chemotherapy may be used clinically to treat the large number of cyclinD1 deregulated resistant tumors. RNA from three paired parental and cisplatin-resistant TGCT cell lines was extracted and analysed by Affymetrix gene expression microarray profiling (Human Genome U133 plus 2.0 arrays). Expression changes associated with the resistant phenotype were identified by comparing the three cisplatin-resistant derivatives to their parental counterparts.
2010-03-15 | E-GEOD-14231 | biostudies-arrayexpress
Project description:The second leading cause of cancer death for women in the U.S. is breast cancer. Moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or âresistomeâ of etoposide resistant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. RNA from MCF7 and etoposide-resistant MCF7 (MCF7VP) cell lines were hybridized to Affymetrix microarrays. Both samples were run in triplicate
2011-04-08 | E-GEOD-28413 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM), a grade IV astrocytoma, is the most common and aggressive brain tumor in adults, characterized by being highly infiltrative, angiogenic, and resistant to chemotherapy and radiotherapy. In previous works, has been determined that progesterone P4 increases proliferation, migration and invasion of cells derived from human GBMs through the interaction with its intracellular receptor (PR). In breast cancer, there exist evidence that P4 regulates the expression of miRNAs with tumor suppressor or oncogenic action, via the classical PR. The signature of miRNAs affected by P4 treatment in cells derived from human GBMs has not been determined. Therefore, we studied the effect of P4 on miRNAs expression pattern in U251 cells derived from a human GBM.
2020-01-25 | GSE144204 | GEO
Project description:Tumors of advanced gastric cancer patients were biopsied and subjected to gene expression profiling using the Affymetrix Human Genome U133 Plus 2.0 Arrays. Patients were then segregated into G1, G2 or G3 groups based on their tumor genomic profiles. Patients in the G1 and G3 cohorts were assigned SOX (oxaliplatin plus S-1) chemotherapy whereas those in the G2 cohort were given SP (cisplatin plus S-1) regimen. This bench-to-bedside effort indicated the feasibility of using molecular profiling to tailor treatment for advanced gastric cancer.
2018-07-31 | GSE100935 | GEO