HSP90 inhibitor resistant cell line
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ABSTRACT:
PROVIDER: EGAS00001006381 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Analysis of the acquired copy number profile in K562 cell which got resistant against HSP90 inhibitors.
| EGAS00001006385 | EGA
Project description:K562 cells were treated with different HSP90 inhibitors (PuH71 and Coumermycin A1) and the CNV profil was compared to the parental K562 (untreated). In addition, the CNV profile of HSP90AB1 knockout K562 cells was analyzed.
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Project description:Comparative label free quantitative proteomic analysis using SWATH-MS has been carried out for K562 cells treated with Imatinib (S+IM) against untreated K562 (S) as well as imatinib resistant K562 cells (R). Compariosn of S+IM vs R constitutes Dataset 1 while that of S vs S+IM constitutes dataset 2
2019-06-14 | PXD009686 | Pride
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
Project description:The Sanger Institute has the largest collection of genetically-characterised cancer cell lines world-wide (we have collected >1000 human cancer cell lines which are being screened against >400 cancer therapeutics (http://www.sanger.ac.uk/genetics/CGP/translation). These lines have been characterized to the level of gene copy number, gene expression and cancer gene mutation sequence data. This has enabled us to select melanoma lines with varying BRAF mutational status and that show sensitivity to a range of BRAF inhibitors. Sensitive lines are being used to generate resistant clones by serial exposure to increasing concentrations of BRAF and MEK inhibitors and these are being characterised by genome-wide copy number analysis as well as by whole exome sequencing.
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Project description:After over 25cycle and 18month's induction of shikonin, K562 cell show maginal resistance to shikonin but great change in gene expression We use microarray to detect the global gene expression change of shikonin resistant cell K562 cell was treated by 4uM shikonin for 4hours, then allowed to die and grow back in fresh medium. Once recovered, cells were immidiatly subjected to another treatment.
2011-12-10 | E-GEOD-34298 | biostudies-arrayexpress
Project description:Proteasome inhibitor (PI) resistance remains a central challenge in multiple myeloma. To identify pathways mediating resistance, we first mapped proteasome-associated genetic co-dependencies. We identified cytosolic heat shock protein 70 (HSP70) chaperones as potential targets, consistent with proposed mechanisms of myeloma tumor cells overcoming PI-induced stress. These results led us to explore allosteric HSP70 inhibitors (JG compounds) as myeloma therapeutics. We showed these compounds exhibit increased efficacy against acquired and intrinsic PI-resistant myeloma models, unlike HSP90 inhibition. Surprisingly, shotgun and pulsed-SILAC mass spectrometry found that JGs have the most pronounced effect on the proteome not through inhibiting cytosolic HSP70s but instead through mitochondrial-localized HSP70, HSPA9/mortalin, destabilizing the 55S mitoribosome. Analysis of myeloma patient data further supports strong effects of global proteostasis capacity, and particularly HSPA9 expression, on PI response. Our results characterize myeloma proteostasis networks under therapeutic pressure while motivating further investigation of HSPA9 as a specific vulnerability in PI-resistant disease.
2022-05-27 | PXD032030 | Pride
Project description:MCF-7aro cells were used to generate a cell culture model system that is resistant to 3 aromatase inhibitors (AIs), letrozole, anastrozole and exemestane. For comparison, the MCF-7aro cells were also used to generate the tamoxifen-resistant cells as well as long-term estrogen deprived, LTEDaro. Affymetrix microarray analysis was performed to determine changes in gene expression that are unique to AI-resistance. Experiment Overall Design: For control purposes, MCF-7aro cells were cultured without any hormone or inhibitor as well as a hormone-only control (T-only). Resistant cells were grown in the presence of testosterone, T+LET R (letrozole), T+ANA R (anastrozole), T+EXE R (exemestane), T+TAM R (Tamoxifen). In addition, testosterone-free resistant lines were generated, LTEDaro, ANA R and EXE R. 6 replicates were generated for the hormone-containing resistant lines and 3 replicates for the hormone-free resistant lines.
2008-04-04 | E-GEOD-10911 | biostudies-arrayexpress
Project description:The aim of the analysis is to study the relationship between tyrosine kinase inhibitor (TKI) resistance mechanism and phenotypic plasticity in the TKI-resistant and parental chronic myeloid leukemia K562 cell lines, in the presence and absence of imatinib. Results provide insight into the molecular mechanisms underlying the acquisition of cancer cell plasticity.
2020-04-14 | GSE120932 | GEO
Project description:After over 25cycle and 18month's induction of shikonin, K562 cell show maginal resistance to shikonin but great change in gene expression We use microarray to detect the global gene expression change of shikonin resistant cell
2011-12-10 | GSE34298 | GEO