Expression data changes induced by 3D conditions in T-ALL cells [CCRF-CEM cells]
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PROVIDER: PRJNA788450 | ENA |
REPOSITORIES: ENA
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Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed micro-RNA on two different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line.
2015-11-04 | E-GEOD-74632 | biostudies-arrayexpress
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed comparative Genome hybridization (arrayCGH) for DNA copy number analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compared to the parental CCRF-CEM wildtype cell line and reference DNA.
2015-11-04 | E-GEOD-74633 | biostudies-arrayexpress
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed. We performed gene expression microarray analysis on four different bortezomib resistant subclones of the CCRF-CEM cell line. The resistant subclones were compaired to treated and untreated the parental CCRF-CEM wildtype cell line.
2015-11-04 | E-GEOD-74634 | biostudies-arrayexpress
Project description:3D constrained conditions promoted H3K4 methylation in ALL cells that altered the global chromatin configuration and transcriptional changes related to cell cycle and DNA replication.
2023-12-13 | GSE190771 | GEO
Project description:Parental and resistant CCRF-CEM cells were treated for 48 hr with a sublethal dose of FK866 (5 nM) or DMSO (Mock, control treatment). This comparison enables the identification of the specific transcriptional alterations induced by FK866 in parental or resistant cells. Keywords: transcriptome profiling, FK866, drug resistance
2018-03-14 | GSE96636 | GEO
Project description:Two human acute lymphoblastic leukemia cell lines (Molt-4 and CCRF-CEM) were treated with direct (A-769662) and indirect (AICAR) AMPK activators. Molt-4 and CCRF-CEM cells were obtained from ATCC (CRL-1582 and CCL-119). Control samples were used for the analysis of metabolic differences between cell lines. Therefore the data was analyzed in combination with, metabolomic data, and the genome-scale reconstruction of human metabolism. For experiments cells were grown in serum-free medium containing DMSO (0.67%) at a cell concentration of 5 x 105 cells/mL.
2014-12-31 | GSE53123 | GEO
Project description:To study the interplay between GFI1 and IKAROS in T-cell Acute Lymphoblastic Leukemia (T-ALL), we applied ChIP-Seq to CCRF-CEM cells expressing 3XFLAG-tagged GFI1 OR IKAROS under doxycycline-inducible control.We found these two protiens associated with common genes, including genes associated with T cell development.
2021-10-31 | GSE160181 | GEO
Project description:It has been shown previously that glucocorticoids exert a dual mechanism of action, entailing cytotoxic, mitogenic as well as cell proliferative and anti-apoptotic responses, in a dose-dependent manner on CCRF-CEM cells at 72 h. Early gene expression response implies a dose-dependent dual mechanism of action of prednisolone too, something reflected on cell state upon 72 h of treatment. In this work, a generic, computational microarray data analysis framework is proposed, in order to examine the hypothesis whether CCRF-CEM cells exhibit an intrinsic or acquired mechanism of resistance and to investigate the molecular imprint of this, upon prednisolone treatment. The experimental design enables the examination of both the dose (0 nM, 10 nM, 22 uΜ, 700 uΜ) effect of glucocorticoid exposure and the dynamics (early and late, namely 4 h, 72 h) of the molecular response of the cells at the transcriptomic layer. In this work we demonstrated that CCRF-CEM cells may attain a mixed mechanism of response to glucocorticoids, however, there is clear evidence predicating towards an intrinsic mechanism of resistance. More specifically, at 4 h prednisolone appeared not to perform its expected function by down-regulating apoptotic genes, which is re-enforced by mechanisms, which down-regulate other sets of apoptotic genes. Also, low and high prednisolone concentrations up-regulates metabolic and signal-transduction related genes in both time points, thus grounding for a cell proliferation machinery. In addition, regulation of NF-κB-related genes implies an inherent mechanism of resistance through the established link of NF-κB inflammatory role and GC-induced resistance. The analysis framework applied here allows derivation of regulatory mechanisms activated by prednisolone through identification of early responding sets of genes. On the other hand, study of the prolonged exposure to glucocorticoids (72 h exposure) highlights the effect of homeostatic feedback mechanisms of the treated cells. Overall, it appears that CCRF-CEM cells in this study exhibit a diversified, combined pattern of intrinsic and acquired resistance to prednisolone, yet with a tendency towards inherent resistant characteristics, through activation of different molecular courses of action.
2011-03-26 | GSE28154 | GEO
Project description:The beneficial effects of glucocorticoids (GCs) in acute lymphoblastic leukemia (ALL) are based on their ability to induce apoptosis. Omics technologies such as DNA microarray analysis are widely used to study the changes in gene expression and have been successfully implemented in biomarker identification. In addition, time series studies of gene expression enable the identification of correlations between kinetic profiles of glucocorticoid receptor (GR) target genes and diverse modes of transcriptional regulation. This study presents a genome-wide microarray analysis of both our and published Affymetrix HG-U133 Plus 2.0 data in GCs-sensitive and -resistant ALL. GCs-sensitive CCRF-CEM-C7-14 cells were treated with dexamethasone at three time points (0 h, 2 h and 10 h). The treated samples were then compared to the control (0 h). Dexamethasone-treated CCRF-CEM-C7-14 samples were divided into 3 groups based on time points: the untreated control (0 h), 2 h and 10 h.
2012-09-01 | E-GEOD-39338 | biostudies-arrayexpress
Project description:Bortezomib is a proteasome inhibitor used in severel different hematological malignancies. Resistance to this drug is still poorly understood. In order get more insight in the resistance mechanism, we developed several bortezomib resistant subclones of the CCRF-CEM T-ALL cell line. On these subclones comparative Genome hybridization (arrayCGH) for DNA copy number analysis gene expression and micro-RNA expression arrays were performed.
2015-11-04 | GSE74633 | GEO