Homo sapiens
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ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-39338
PROVIDER: PRJNA170666 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE39335: Expression data from glucocorticoid-treated ALL (BCR-ABL patients) GSE39338: Expression data from glucocorticoid-treated ALL (CCRF-CEM-C7-14 cells) Refer to individual Series
2012-09-01 | E-GEOD-39339 | biostudies-arrayexpress
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:Expression data from glucocorticoid-treated ALL (CCRF-CEM-C7-14 cells)
2015-09-29 | E-GEOD-39338 | ExpressionAtlas
Project description:The efficacy of glucocorticoid receptor modulation is well established in Acute Lymphoblastic Leukemia(ALL) but the response remains heterogeneous and limited by emergence of drug resistance. Here we use, two clonally-derived cell lines (CEM-C1 and CEM-C7) from a 3-year-old T-cell ALL patient, as a model system to understand the mechanisms of drug resistance in these cell lines; the clone CEM-C1 is resistant to dexamethasone-induced apoptosis and CEM-C7 is sensitive. We performed ATACseq and RNAseq to query for TF binding motifs present in the open regions of the chromatin and expression levels of TFs that could recognize the identified motifs. We are experimentally validating our hypothesis that depletion of the TFs identified, either singly or in combination, in CEM-C7 cells will cause dexamethasone resistance in CEM-C7 cells.
2021-07-20 | GSE102038 | 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). Arrays were obtained from 10 children with Philadelphia positive (Ph+) ALL treated uniformly. They were categorized as good risk if the marrow had <25% blasts after 8 days of therapy without imatinib and poor risk if the blast count was >25%. During this time they received 8 days of Dex and 1 dose each of anthracycline, vincristine and L-Asparaginase, according to the EsphALL protocol. The samples were analysed at day 17 and compared to the untreated (day 0) samples.
2012-09-01 | E-GEOD-39335 | biostudies-arrayexpress
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:Gene expression data of glucocorticoid resistant and sensitive acute lymphoblastic leukemia cell lines for the article: Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases (PFKFBs) in glucocorticoid-induced apoptosis of acute lymphoblastic leukemia cells Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and constitute a central component in the therapy of lymphoid malignancies, most notably childhood acute lymphoblastic leukemia (ALL). PFKFB2 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-2), a kinase controlling glucose metabolism, was identified by us previously as GC response gene in expression profiling analyses performed in children with ALL during initial systemic GC mono-therapy. Since deregulation of glucose metabolism has been implicated in apoptosis induction, this gene and its relatives PFKFB1, 3, and 4 were further analyzed. Expression analyses in additional ALL children, non-leukemic individuals and leukemic cell lines confirmed frequent PFKFB2 induction by GC in most systems sensitive to GC-induced apoptosis, particularly in T-ALL cells. The 3 other family members, in contrast, were not or weakly expressed (PFKFB1 and 4) or not induced by GC (PFKFB3). Conditional PFKFB2 over-expression in the CCRF-CEM T-ALL in vitro model revealed that its 2 splice variants (15A and 15B) did not have any detectable effect on survival or cell cycle progression. Moreover, neither PFKFB2 splice variant significantly affected sensitivity to, or kinetics of, GC-induced apoptosis. Our data suggest that, at least in the model system investigated, PFKFB2 is not an essential upstream regulator of the anti-leukemic effects of GC. Generation of the GC sensitive and resistant clones is described in Parson et al. FASEB J 2005 (Pubmed id 15637111). In brief GC sensitive clones were generated by limiting dilution subcloning from the GC sensitive T-ALL cell line CCRF-CEM-C7H2. To generate GC resistant clones the CCRF-CEM-C7H2 cell line was clutured in the presence of 10E-7 M dexametasone. Gene expression profiles of glucocorticoid (GC) resistant and sensitive T-ALL cells during GC treatment and corresponding control samples (cells treated with carrier control). GC induced regulation of PFKFB2 was determined in the various cell lines based on the expression intensities of the corresponding probe sets in GC treated and control samples.
2011-02-01 | E-GEOD-22152 | biostudies-arrayexpress
Project description:Bortezomib resistance in CCRF-CEM cell line [GEP]
| PRJNA301042 | ENA
Project description:Bortezomib resistance in CCRF-CEM cell line [miRNA]
| PRJNA301041 | ENA