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Anthracycline resistance in four human cancer cell lines (HGU95A)

ABSTRACT: Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: cell type comparison

ORGANISM(S): Homo sapiens

PROVIDER: GSE3927 | GEO | 2010/04/15

SECONDARY ACCESSION(S): PRJNA94339

REPOSITORIES: GEO

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Anthracycline resistance in four human cancer cell lines (HGU95A)

Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: cell type comparison See Summary. Note: this series includes Affymetrix HGU95A chips (difference between resistant and parental cell lines).

2010-04-15 | E-GEOD-3927 | biostudies-arrayexpress

Anthracycline treatment and resistance in four human cancer cell lines

Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: superSeries This reference Series links data in the following related Series: GSE3926 Anthracycline treatment and resistance in four human cancer cell lines (HGU133A) GSE3927 Anthracycline resistance in four human cancer cell lines (HGU95A)

2010-04-14 | E-GEOD-3929 | biostudies-arrayexpress

Anthracycline treatment and resistance in four human cancer cell lines (HGU133A)

Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a âvirtual arrayâ composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. Keywords: cell type and treatment comparison See Summary. Note: this series includes Affymetrix HGU133A chips (difference between resistance and treatment response).

2010-04-27 | E-GEOD-3926 | biostudies-arrayexpress

Anthracycline treatment and resistance in four human cancer cell lines

Project description:Reliable clinical tests for predicting cancer chemotherapy response are not available and individual markers failed to correctly predict resistance against anticancer agents. We hypothesized that gene expression patterns attributable to chemotherapy-resistant cells can be used as a classification tool for chemoresistance and provide novel candidate genes involved in anthracycline resistance mechanisms. We contrasted the expression profiles of 4 different human tumor cell lines of gastric, pancreatic, colon and breast origin and of their counterparts resistant to the topoisomerase inhibitors daunorubicin or doxorubicin. We also profiled the sensitive parental cells treated with doxorubicin for 24h. We interrogated Affymetrix HGU133A and U95A arrays independently. We applied two independent methods for data normalization and used Prediction Analysis of Microarrays (PAM) for feature selection. In addition, we established data sets related to drug resistance by using a “virtual array” composed of features represented on both types of oligonucleotide arrays. We identified 71 candidate genes associated with doxorubicine/daunorubicine resistance. To validate the microarray data, we also analyzed the expression of 12 selected genes by quantitative RT-PCR or immunocytochemistry, respectively. While the comparison of drug-sensitive versus drug-resistant cells yields candidates associated with drug resistance, the 24h treatment of sensitive parental cells produced a distinct transcriptional profile related to short-term drug effects. This SuperSeries is composed of the SubSeries listed below.

2010-04-15 | GSE3929 | GEO

Anthracycline treatment and resistance in four human cancer cell lines (HGU133A)

2010-04-15 | GSE3926 | GEO

Global gene expression analysis of anthracycline-resistant breast cancer cell lines

Project description:Drug resistance in breast cancer is the major obstacle to a successful outcome following chemotherapy treatment. While upregulation of multidrug resistance (MDR) genes is a key component of drug resistance in multiple cancers, the complexity and hierarchy of non-MDR driven drug resistance pathways are still largely unknown. The aim of this study was to identify pathways contributing to anthracycline resistance using isogenic drug resistant breast cancer cell lines. We generated isogenic MDA-MB-231, MCF7, SKBR3 and ZR-75-1 epirubicin-resistant breast cancer cell lines, which were cross-resistant to doxorubicin and SN-38; the SKBR3 cell line was also resistant to taxanes. Epirubicin-resistant cells were morphologically different from native cells, and had alterations in apoptosis and cell cycle profile. Using gene expression and small-molecule inhibitor analyses we identified deregulation of histone H2A and H2B genes in all four cell lines. These genes contribute to several biological pathways, which include cell cycle, chromosomal maintenance, epigenetics, RNA and mitochondrial transcription. Histone deacetylase and cell cycle/DNA damage small molecule inhibitors reversed resistance and were cytotoxic for all four epirubicin-resistant cell lines confirming that histone and cell cycle pathways are associated with epirubicin resistance. This study has established model systems for investigating drug resistance in all four breast cancer subtypes and revealed key pathways that contribute to anthracycline resistance. The global gene expression analysis included 4 parental (anthracycline sensitive) and 4 resistant breast cancer cell lines, in biological triplicates.

2014-01-24 | E-GEOD-54326 | biostudies-arrayexpress

Transcription profiling of 5 human parental cell lines and 3 drug resistant variants by culturing the former continuously in the presence of cytotoxic drug doxorubicin

Project description:Title: Analysis of gene expression changes involved in the development of acquired drug resistance.<br> Description: In vitro model of drug resistance consisting of 5 parental cell lines and 3 drug resistant variants by culturing the former continuously in the presence of cytotoxic drug doxorubicin. Model used to identify genes involved in the drug resistant phenotype.

2006-09-01 | E-MIMR-11 | biostudies-arrayexpress

Sustained Activation of Non-canonical NF-kB Signalling Drives Glycolytic Reprogramming in Doxorubicin-resistant DLBCL

Project description:The transcriptomic profiles of two resistant (HT and OCI-LY3) and two sensitive (SUDHL5 and OCI-LY19) DLBCL cell lines before and after doxorubicin treatment were analysed by RNA-seq. To further investigate the molecular basis underlying the development of doxorubicin resistance, acquired doxorubicin-resistant cells (OCI-LY19R) were generated by periodically treating the parental doxorubicin-sensitive OCI-LY19 cells (OCI-LY19S) with increasing doses of doxorubicin over a prolonged period till its IC50 exceeded 200 nM. RNA-seq analysis was then performed using OCI-LY19R and OCI-LY19S cell lines to examine the transcriptomic changes following acquisition of doxorubicin resistance.

2022-12-01 | GSE215900 | GEO

RNA-Seq of neuroblastoma Th-MYCN mouse model, samples sensitive to chemotherapy, and those with chemotherapy resistance

Project description:Some neuroblastoma patients relapse after chemotherapy. Here, a Th-MYCNCPM32 mouse model usually have spontaneously tumours which are sensitive to chemotherapy. By treating mice with consecutive cycles of sublethal cyclophosphamide (CPM) using a personal dose escalation protocol (PDE), resistant tumours may develop. This experiment aims to compare the expression profiles (RNA-Seq) of sensitive and resistant MYCN driven tumours in order to understand the mechanisms behind resistance. Samples also presented cross-resistance to vincristine and doxorubicin.

2018-09-30 | E-MTAB-5858 | biostudies-arrayexpress

Expression data from doxorubicin-resistant hepatoma cells

Project description:Transarterial chemoembolization or systemic chemotherapy with doxorubicin has been the treatment of choice for unresectable hepatocellular carcinoma (HCC) conferring the best survival benefit. However, HCC is notorious for its predisposition to develop therapeutic tolerance. Thus, Affymetrix microarray analysis was performed on doxorubicin-resistant hepatoma cells to identify the drug resistance-related genes. The RNA isolated from primary hepatoma cells and their doxorubicin-resistant counterparts, then subjected to Affymetrix microarray analysis to identify the differential expression profiles of drug resistance-related genes.

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