Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA118859 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Multiple Myeloma (MM) remains incurable despite novel therapies, suggesting the need for further identification of factors mediating tumorigenesis and drug resistance. We performed microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells.
2009-07-31 | GSE17407 | GEO
Project description:Multiple Myeloma (MM) remains incurable despite novel therapies, suggesting the need for further identification of factors mediating tumorigenesis and drug resistance. We performed microarray analysis to identify the molecular mechanisms whereby pDCs confer growth and drug resistance in MM cells. Comparsion of MM cells in the presence and absence of pDCs (plasmacytoid dendritic cells)
2009-07-31 | E-GEOD-17407 | biostudies-arrayexpress
Project description:Malignant melanoma (MM) remains a therapeutic challenge on account of extreme primary resistance to apoptosis and fated acquired chemoresistance. In the current context of molecular classification of MM, the understanding of molecular mechanisms giving rise to these resistances should drive therapeutic choice trough personalized medicine. In order to study mechanisms of MM acquire resistance to VAs, we previously established three VA-resistant cell lines, CAL1R-VCR, CAL1R-VDS, and CAL1R-VRB, by long time exposure of the CAL1-wt MM cell line to IC50 (4nM) of VCR, VDS and VRB respectively. CAL1R-VAs cell lines consisted of polyclonal populations to respect biological diversity of tumour. Then, we searched for determine the resistance process impact on MM cells. We thus performed genome-wide analyses based on comparison of global transcriptomic profile of CAL1R-VAs cells to CAL1-wt. In this way, RNA extracted from each cell line was hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. After hybridization, microarray data were processed with Robust Multi-array Average (RMA) algorithm. We then performed bioinformatic analyses of microarray data and in vitro investigations in the aim to identify genes and pathways that might predict drug resistance.
2014-09-03 | GSE61007 | GEO
Project description:Purpose:To identify resistance mechanisms for the chemotherapeutic drug fludarabine in chronic lymphocytic leukemia (CLL), as innate and acquired resistance to fludarabine-based chemotherapy represents a major challenge for long-term disease control. Methods: We employed piggyBac transposon-mediated mutagenesis, combined with next-generation sequencing, to identify genes that confer resistance to fludarabine in a human CLL cell line. Results: RNA-seq profiling of fludarabine-resistant cells suggested deregulated MAPK signaling as involved in mediating drug resistance in CLL. To address if the fludarabine-resistant HG3 cells were transcriptionally different at a global level compared to their parental cells, we performed RNA-sequencing of three pairs of HG3 pools
2016-03-31 | E-GEOD-75844 | biostudies-arrayexpress
Project description:Purpose:To identify resistance mechanisms for the chemotherapeutic drug fludarabine in chronic lymphocytic leukemia (CLL), as innate and acquired resistance to fludarabine-based chemotherapy represents a major challenge for long-term disease control. Methods: We employed piggyBac transposon-mediated mutagenesis, combined with next-generation sequencing, to identify genes that confer resistance to fludarabine in a human CLL cell line. Results: RNA-seq profiling of fludarabine-resistant cells suggested deregulated MAPK signaling as involved in mediating drug resistance in CLL.
2016-03-31 | GSE75844 | GEO
Project description:Here we show that the human fungal pathogen Mucor circinelloides develops spontaneous resistance to the antifungal drug FK506 via two distinct mechanisms. One involves Mendelian mutations that confer stable drug resistance and the other via an epigenetic RNA interference (RNAi)-mediated pathway that results in unstable drug resistance. The peptidyl-prolyl isomerase FKBP12 interacts with FK506 to form a complex that inhibits the protein phosphatase calcineurin. In M. circinelloides, inhibition of calcineurin by FK506 blocks the transition to hyphae and enforces yeast growth. Mutations in the fkbA gene encoding FKBP12 or the calcineurin cnbR or cnaA genes confer FK506 resistance, restoring hyphal growth in the presence of this drug. In parallel, RNAi is spontaneously triggered to silence the FKBP12 fkbA gene, giving rise to drug-resistant epimutants. FK506-resistant epimutants readily reverted to the drug-sensitive wild type (WT) phenotype when selection was released by growth without drug. High-throughput small RNA (sRNA) sequencing showed abundant sRNA antisense to fkbA only in the epimutants and not in the WT or revertant strains. Analysis of RNAi mutants revealed components required for the establishment of drug resistant epimutants as well as other factors that constrain or reverse the epimutation pathway. Silencing involves generation of a double stranded RNA trigger intermediate using the fkbA mature mRNA as template. These results uncover a novel epigenetic RNAi-based epimutation mechanism controlling phenotypic plasticity, with possible implications for antimicrobial drug resistance and RNAi regulatory mechanisms in fungi and other eukaryotes.
2014-07-22 | GSE56353 | GEO
Project description:Malignant melanoma (MM) remains a therapeutic challenge on account of extreme primary resistance to apoptosis and fated acquired chemoresistance. In the current context of molecular classification of MM, the understanding of molecular mechanisms giving rise to these resistances should drive therapeutic choice trough personalized medicine. In order to study mechanisms of MM acquire resistance to VAs, we previously established three VA-resistant cell lines, CAL1R-VCR, CAL1R-VDS, and CAL1R-VRB, by long time exposure of the CAL1-wt MM cell line to IC50 (4nM) of VCR, VDS and VRB respectively. CAL1R-VAs cell lines consisted of polyclonal populations to respect biological diversity of tumour. Then, we searched for determine the resistance process impact on MM cells. We thus performed genome-wide analyses based on comparison of global transcriptomic profile of CAL1R-VAs cells to CAL1-wt. In this way, RNA extracted from each cell line was hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. After hybridization, microarray data were processed with Robust Multi-array Average (RMA) algorithm. We then performed bioinformatic analyses of microarray data and in vitro investigations in the aim to identify genes and pathways that might predict drug resistance. Melanoma model: CAL1 cell line. Treatments: vinorelbine (VRB), vincristine (VCR), vindesine (VDS). Etablishment of 3 resistant cell lines by long time exposure to vinka-alkaloids (4nM, 6-12 months): CAL1R-VRB, CAL1R-VCR, CAL1R-VDS. RNA extracted from a pooled population of each cell line were hybridized to Affimetrix HG-U133 Plus 2.00 GeneChips. Then, microarray data were processed with Robust Multi-array Average (RMA) algorithm.
2014-09-03 | E-GEOD-61007 | biostudies-arrayexpress
Project description:Multiple myeloma (MM) remains incurable due to drug resistance. Ribosomal protein S3 (RPS3) has been identified as a non-Rel subunit of NF-κB. However, the detailed biological roles of RPS3 remain unclear. Here, we report for the first time that RPS3 is necessary for MM survival and drug resistance. RPS3 was highly expressed in MM, and knockout of RPS3 in MM inhibited cell growth and induced cell apoptosis both in vitro and in vivo. Overexpression of RPS3 mediated the proteasome inhibitor resistance of MM and delayed the survival of MM tumour-bearing animals. Moreover, our present study found an interaction between RPS3 and the thyroid hormone receptor interactor 13 (TRIP13), an oncogene related to MM tumorigenesis and drug resistance. We demonstrated that the phosphorylation of RPS3 was mediated by TRIP13 via PKCδ, which played an important role in activating the canonical NF-κB signalling and inducing cell survival and drug resistance in MM. Notably, the inhibition of NF-κB signalling by the small-molecule inhibitor targeting TRIP13, DCZ0415, was capable of triggering synergistic cytotoxicity when combined with bortezomib in drug-resistant MM. This study identifies RPS3 as a novel biomarker and therapeutic target in MM.
2023-08-18 | GSE240978 | GEO
Project description:We generated azacitidine (AZA)- and decitabine (DAC)-resistant (AZA-R and DAC-R, respectively) cells from drug-sensitive ATL cell lines TL-Om1 and MT-2 via long-term drug exposure. To identify molecular mechanisms responsible for acquired resistance, we performed transcriptome analysis using Clariom S microarray.
2021-11-30 | GSE166980 | GEO
Project description:The general objectives are to evaluate activity and the safety of regorafenib in a population of patients bearing advanced, refractory colorectal cancers and to explore the different downstream molecular pathways to identify tumor response and resistance mechanisms.
| 2150618 | ecrin-mdr-crc