Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA104387 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from glucocorticoid-treated ALL (CCRF-CEM-C7-14 cells)
2025-01-24 | E-GEOD-39338 | ExpressionAtlas
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. Experiment Overall Design: CEM-C1 cells were treated with 10 nM rapamycin for 3 hours and compared to DMSO treated cells
2008-06-14 | E-GEOD-5822 | biostudies-arrayexpress
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. Experiment Overall Design: CEM-C1 cells were treated with 10 nM rapamycin or DMSO and harvested for microarray analysis at 24 hours
2008-06-14 | E-GEOD-5821 | biostudies-arrayexpress
Project description:Drug resistance remains a major obstacle to successful cancer treatment. Here we use a novel approach to identify rapamycin as a glucocorticoid resistance reversal agent. A database of drug-associated gene expression profiles was screened for molecules whose profile overlapped with a gene expression signature of glucocorticoid (GC) sensitivity/resistance in Acute Lymphoblastic Leukemia (ALL) cells. The screen indicated the mTOR inhibitor rapamycin profile matched the signature of GC-sensitivity. We thus tested the hypothesis that rapamycin would induce GC sensitivity in lymphoid malignancy cells, and found that it sensitized cells to glucocorticoid induced apoptosis via modulation of antiapoptotic MCL1. These data indicate that MCL1 is an important regulator of GC-induced apoptosis, and that the combination of rapamycin and glucocorticoids has potential utility in ALL. Furthermore this approach represents a novel strategy for identification of promising combination therapies for cancer. This SuperSeries is composed of the following subset Series:; GSE5820: Gene expression-based chemical genomics identifies rapamycin as a modulator of MCL-1 and glucocorticoid resistance; GSE5821: Rapamycin treatment of CEM_C1 cells 24 hours; GSE5822: Rapamycin treated CEM-C1 cells 3 hours Experiment Overall Design: Refer to individual Series
2008-11-06 | E-GEOD-5824 | biostudies-arrayexpress
Project description:RNA-seq of OE19 cells treated with siNT or siKLF5 for 72 hours
2025-01-16 | E-MTAB-8446 | ExpressionAtlas
Project description:RNA-seq of OE19 cells treated with siNT or siERBB2 for 72 hours
2025-01-16 | E-MTAB-8579 | 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:Hematopoietic stem cells from mice treated with G-CSF or saline alone for 36 hours
2015-08-04 | E-GEOD-55093 | ExpressionAtlas
Project description:Human CEM Cells: Control vs. 2h or 4.5h Cluvenone Treated
| PRJNA131757 | ENA