Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

4da0d358-1544-4812-a29a-6b30a85f5b0c - samples

ABSTRACT: K562 cell line has been treated with two different HSP90 inhibtors. After resistance clones emerged, they have been genetically characterized using WES in comparison to the parental K562 cell line.

PROVIDER: EGAD00001009051 | EGA |

REPOSITORIES: EGA

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of Imatinib and PD166326 resistant cell lines

Project description:A comparison between parental K562 cells (CML) and two clones derived from this cell line : ImaR and PDR which are resistant against Imatinib mesylate and PD166326 respectively , two inhibitors of BCR-ABL. Keywords: gene expression, comparison

2009-06-01 | GSE10382 | GEO

Transcriptomic analysis of trametinib-resistant HCT116 colorectal carcinoma cells compared to the parental control cells

Project description:HCT116 cells were treated with with increasing concentrations of trametinib over 2 months. Drug-resistant clones emerged and were cultured in the presence of 30 nmol/L trametinib. These cells exhibited a greater than 10-fold increase in the GI50 for trametinib compared to the parental cell line. RNA-seq of the resistant clone HCT116_R4 versus the parental cells identified differentially expressed genes potentially involved in resistance.

2018-10-23 | GSE118490 | GEO

Expression of BRAF inhibitor resistant colon cancer lines

Project description:Colon cancer cell lines with partial sensitivity to the BRAF inhibitor PLX4720 were grown in increasing concentration of the drug to develop acquired resistance. Gene expression was performed for comparison of the resistant clones to the parental lines. Colon cancer cell lines with partial sensitivity to the BRAF inhibitor PLX4720 were grown in increasing concentration of the drug to develop acquired resistance. Gene expression was performed for comparison of the resistant clones to the parental lines.

2012-09-15 | E-GEOD-34299 | biostudies-arrayexpress

Expression of BRAF inhibitor resistant colon cancer lines

2012-09-15 | GSE34299 | GEO

Basal mRNA expression levels of single-cell derived FaDu clones with cisplatin-sensitive / resistant phenotype

Project description:The extent of intratumoral heterogeneity, the subclonal structures and the mechanisms of treatment-induced clonal selection by cisplatin was investigated in the squamous cell carcinoma cell line model FaDu. We picked 96 single cell-derived clones from the cisplatin-sensitive parental FaDu cell line. After expansion as separate cultures, these clones were tested for their sensitivity to CDDP. By this approach, we isolated individual cell clones that were primarily resistant (clones 5 & 78) and others that showed high sensitivity to CDDP (clones 46 & 54). Basal mRNA expression levels associated with CDDP sensitivity / resistance were determined in two independent microarray analyses.

2017-12-04 | E-MTAB-6022 | biostudies-arrayexpress

Transcriptional adaptation and enhancer rewiring promote metabolic resistance in BRAFmutated multiple myeloma (bulkRNA-seq)

Project description:Purpose: We examined how transcriptional state changes relate to clonal selection as BRAF inhibitor resistance develops in BRAF-mutated myeloma. Methods: To this end we generated three single-cell clones from U266, a BRAFK601N -mutated myeloma cell line and DP6- a BRAFV600E myeloma cell line. All three U266 and DP6 clones were subjected to long-term dabrafenib treatment at their established IC50 doses (U266: 10uM, DP6 1nM). Bulk RNA-seq was performed before treatment, day 7, day 14, day 42 and at time of resistance. Results: Transcriptional adaptation after seven days was homogeneous for all clones, but was different across both cell lines. Oxidative phosphorylation (OxPhos) emerged as the most consistently enriched signaling pathway in persistent cells from both cell lines as compared to baseline. Conclusions: BRAF inhibition in BRAF-mutated myeloma cells leads to transcriptional reprogramming with induction of OxPhos-related genes within a brief period of time.

2022-03-13 | GSE168950 | GEO

Distinct epigenetic profiles at the cytosine modification level define epithelial-to-mesenchymal cell-state transitions

Project description:Genome wide DNA methylation and hydroxymethylation profiling of 6 isolated single cell clones and the parental (SUM149-PT) cell line. The Illumina Infinium Human MethylationEPIC Beadchip was used to obtain DNA methylation and hydroxymethylation profiles across approximately 850,000 CpGs in 6 isolated single cell clones that represent the phenotypes of the epithelial-to-mesenchymal spectrum along with the parental (SUM149-PT) cell line. Isolated single cell clones represent varying phenotypes of the epithelial-to-mesenchymal transition. Detailed isolation and characterization methods can be found in Brown et al, 2021. https://doi.org/10.1101/2021.03.17.434993

2022-05-27 | GSE181036 | GEO

Impact of the bone microenvironment on phenotypic plasticity of ER+ breast cancer cells [exome-seq]

Project description:Whole Exome Sequencing (WES) was used to evaluate genomic alterations between parental cells, SCPs (Single Cell-derived Subpopulations) and bone-entrained cells.

2021-04-16 | GSE161181 | GEO

Changes in the expression of miR-381 and miR-495 are inversely associated with the expression of the MDR1 gene and development of multi-drug resistance

Project description:Multidrug resistance (MDR) frequently develops in cancer patients exposed to chemotherapeutic agents and is usually brought about by over-expression of P-glycoprotein (P-gp) which acts as a drug efflux pump. MiRNAome profiling using next-generation sequencing identified differentially expressed microRNAs (miRs) between parental K562 cells and MDR K562 cells (K562/ADM) induced by chronic adriamycin treatment. MiRNAome profiling in untreated K562 cells and K562 cells exposed to long-term adriamycin treatment

2013-10-29 | E-GEOD-51774 | biostudies-arrayexpress

RNA sequencing of PC9 and four erlotinib-persister cells derived from PC9

Project description:Given the recent reports on the role of AXL in mediating resistance to EGFR-targeted therapy, we generated cell line models of Erlotinib-resistance to investigate the effect of AXL inhibitors on EGFR TKI resistance. For this, EGFR-mutant PC9 cells were passed through a persister bottleneck by applying strong drug selection pressure to generate drug-tolerant erlotinib persister cells. We created four Erlotinib-resistant clones from one parental population; S1-34, S2-10, S2-17 and S2-30. Whole exome and RNA sequencing analyses were performed to probe the differences in Erlotinib-resistance mechanisms present in these persister-derived Erlotinib-resistant cells.

2022-04-13 | GSE191185 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data