Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA205633 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR868782_1.fastq.gz | Fastqsanger.gz | |||
| SRR868782_2.fastq.gz | Fastqsanger.gz | |||
| SRR868783_1.fastq.gz | Fastqsanger.gz | |||
| SRR868783_2.fastq.gz | Fastqsanger.gz | |||
| SRR868784_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
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Project description:Using two independently derived murine BXH2 cell lines, Ara-C resistant derivatives were developed by exposure to increasing concentrations of Ara-C. Microarray analysis comparing the Ara-C resistant cells to their Ara-C sensitive parental cell lines identified potential genes involved in Ara-C resistance.
2010-03-01 | GSE18322 | GEO
Project description:Using two independently derived murine BXH2 cell lines, Ara-C resistant derivatives were developed by exposure to increasing concentrations of Ara-C. Microarray analysis comparing the Ara-C resistant cells to their Ara-C sensitive parental cell lines identified potential genes involved in Ara-C resistance. Two highly Ara-C-resistant cell lines, B117H and B140H, were derived from Ara-C-sensitive parental cell lines, B117P and B140P. Variations in gene expression between these Ara-C-resistant and -sensitive sets were studied. Three replicates per cell line.
2010-03-07 | E-GEOD-18322 | biostudies-arrayexpress
Project description:Wide inter-individual variation in terms of outcome and toxic side effects of treatment exist among patients with AML receiving chemotherapy with cytarabine (Ara-C) and daunorubicin (Dnr). Drug resistance and relapse are considered major causes of treatment failure. Gene expression profiling was undertaken to address possible mechanisms of Ara-C/Dnr resistance. Based on ex vivo Ara-C cytotoxicity at diagnosis, Ara-C sensitive (IC50 <3uM AraC) and Dnr sensitive samples (IC50 < 0.5 uM) (5 samples each) were included for microarray analysis. These were compared with the samples which were drug resistant ex vivo at diagnosis. Our microarray experiment resulted in indentifying differentially expressed genes under ex vivo Ara-C sensitive as well as Dnr sensitive samples compared to ex vivo Drug resistant samples.
2016-01-02 | GSE52919 | GEO
Project description:Wide inter-individual variation in terms of outcome and toxic side effects of treatment exist among patients with AML receiving chemotherapy with cytarabine (Ara-C) and daunorubicin (Dnr). Drug resistance and relapse are considered major causes of treatment failure. Gene expression profiling was undertaken to address possible mechanisms of Ara-C/Dnr resistance. Based on ex vivo Ara-C cytotoxicity at diagnosis, Ara-C sensitive (IC50 <3uM AraC) and Dnr sensitive samples (IC50 < 0.5 uM) (5 samples each) were included for microarray analysis. These were compared with the samples which were drug resistant ex vivo at diagnosis. Our microarray experiment resulted in indentifying differentially expressed genes under ex vivo Ara-C sensitive as well as Dnr sensitive samples compared to ex vivo Drug resistant samples. One-color experiment,Organism: Homo sapiens, Custom Human Whole Genome 8x60k Array designed by Genotypic Technology Private Limited (AMADID: 27114), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2016-07-04 | E-GEOD-52919 | biostudies-arrayexpress
Project description:Gene Expression Analysis of Ara-C Resistance in AML
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Project description:An RNA-seq study of altered gene expression and mutations in Ara-C resistant acute myeloid leukemia murine cell lines. The analysis of the RNA-seq data led to the identification of a large deletion within the Dck coding sequence of the B117H cell line, which produced an alternatively processed form of Dck mRNA. The RNA-seq analysis also identified the presence of an insertion mutation in Dck in the B140H cell line. The RNA-seq analysis also identified a number of significant expression changes which did not appear in a previous microarray analysis (GSE18322), as well as identified other mutations which may be contributing to Ara-C resistance. Two highly Ara-C resistant cell lines, B117H and B140H were derived from Ara-C sensitive parental cell lines, B117P and B140P. Variations in gene expression as well identification of acquired mutations between these Ara-C resistant/sensitive sets were studied using various RNA-seq analysis tools.
2014-08-13 | E-GEOD-47454 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML) originates from malignant, immature myeloid progenitor cells that differentiate into dysfunctional myeloblasts. While cytarabine (Ara-C) and daunorubicin (DNR)-based chemotherapy regimens are the standard treatments, approximately 10-40% of AML patients under the age of 60 and 40-60% over 60 do not respond, leading to refractory or relapsed (R/R) AML. Targeted chemotherapy for FLT3-ITD mutated R/R AML cells improves response rates and survival outcomes in FLT3-ITD mutated R/R AML patients. However, patients with wild-type FLT3 R/R AML remain therapeutically challenged, with persistent difficulty in finding effective treatments. Better insights on the fundamental understanding of treatment failure in wild-type FLT3 AML cells are needed to enhance therapeutic outcomes. However, precise mechanisms behind the treatment failure remain unclear. This study investigates the mechanisms underlying the failure of Ara-C and DNR-based chemotherapy in wild-type FLT3 R/R AML. Using RHI-1 cells, a wild-type FLT3 AML cell line with Ara-C resistance, we demonstrated that Ara-C resistance-mediated DNR tolerance did not result from reducing the concentration of DNR in RHI-1 cells, but rather from interrupting the cytotoxic mechanisms of DNR through the Ara-C resistance of RHI-1. The down-regulated deoxycytidine kinase (DCK) in RHI-1 cells interrupted mechanisms of Ara-C cytotoxic action. Also, the down-regulation of DCK enhanced mitochondrial metabolic pathways, DNA repair process, and ROS detoxification. Through these pathways, RHI-1 cells exhibit tolerance under DNR treatment. Among these enhanced processes, targeting mitochondrial metabolism, particularly OXPHOS complex I proteins, improved the efficacy of both Ara-C and DNR. Our findings shed light on a potential mechanism underlying the treatment failure and the role of mitochondrial metabolism in wild-type FLT3 R/R AML cells.
2025-05-07 | PXD054797 | Pride
Project description:Acute myeloid leukemia (AML) exhibits a spectrum of responses to chemotherapy, with drug resistance being a significant clinical challenge. This study employs a multi-omics approach, particularly multiplexed single-cell RNA sequencing (scRNA-seq), to characterize the molecular mechanisms underlying drug resistance in AML cells. We identified significant cellular heterogeneity and a dynamic transcriptomic trajectory in AML cells with specific drug treatment, and discovered a reprogramming towards a more stem-like state. Interestingly, Ara-C-resistant KG-1a cells predominantly originated from G2/M subpopulations, indicating a cell cycle-specific resistance mechanism. Our analysis also revealed that epigenetic changes of DNA methylation and chromatin architechture, and altered transcription factor activities were implicated in rapid Ara-C resistance, whereas exomic mutations did not significantly contribute to it. We suggest both intrinsic and acquired resistance mechanisms act together and build a resultant force that aids AML cells in evading therapeutic interventions. The multidimensional changes observed post-treatment showed a complex interplay in the development of drug resistance. This study provides a cellular and molecular portrait of drug response and resistance in AML, offering potential therapeutic targets and a foundation for future research aimed at overcoming chemoresistance.
2025-05-20 | GSE279118 | GEO
Project description:Acute myeloid leukemia (AML) exhibits a spectrum of responses to chemotherapy, with drug resistance being a significant clinical challenge. This study employs a multi-omics approach, particularly multiplexed single-cell RNA sequencing (scRNA-seq), to characterize the molecular mechanisms underlying drug resistance in AML cells. We identified significant cellular heterogeneity and a dynamic transcriptomic trajectory in AML cells with specific drug treatment, and discovered a reprogramming towards a more stem-like state. Interestingly, Ara-C-resistant KG-1a cells predominantly originated from G2/M subpopulations, indicating a cell cycle-specific resistance mechanism. Our analysis also revealed that epigenetic changes of DNA methylation and chromatin architechture, and altered transcription factor activities were implicated in rapid Ara-C resistance, whereas exomic mutations did not significantly contribute to it. We suggest both intrinsic and acquired resistance mechanisms act together and build a resultant force that aids AML cells in evading therapeutic interventions. The multidimensional changes observed post-treatment showed a complex interplay in the development of drug resistance. This study provides a cellular and molecular portrait of drug response and resistance in AML, offering potential therapeutic targets and a foundation for future research aimed at overcoming chemoresistance.
2025-04-01 | GSE279397 | GEO
Project description:Title: Gene Expression in Ara-C Resistance in AML A microarray study of altered gene expression in acute myeloid leukemia cell lines Keywords: cell type comparison Keywords: Expression profiling by array
2005-09-01 | GSE2788 | GEO