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E-GEOD-58266 - Whole-genome GR binding sites and histone acetylation status in pediatric acute lymphoblastic leukemia patient-derived xenografts following dexamethasone treatment in vivo

Status
Released on 18 December 2014, last updated on 2 January 2015
Organism
Homo sapiens
Samples (6)
Protocols (1)
Description
Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). However, the signaling pathways regulating apoptosis in glucocorticoid-treated lymphoid cells remain unclear. In this study, pediatric ALL patient-derived xenograft inherently sensitive to glucocorticoids were exposed to dexamethasone in vivo. Whole-genome GR binding sites and histone acetylation status were detected using chromatin immunoprecipitation sequencing analyses. This provided a global understanding of dexamethasone-induced DNA modulations in ALL cells in vivo, which is likely to be important in the understanding of mechanisms of glucocorticoid response in lymphoid malignancies. One xenograft (ALL-54) was derived from a patient of dexamethasone-good responder. The xenograft was innoculated into 2 NOD/SCID mice, and treated with dexamethasone (15 mg/kg) or vehicle control. Binding of glucocorticoid receptor (GR), histone acetylation and IgG control in spleen-harvest xenograft samples were detected using ChIP-seq.
Experiment type
ChIP-seq 
Contacts
Dominik Beck, Duohui Jing, Jason W Wong, John E Pimanda, Richard B Lock
Citation
Opposing regulation of BIM and BCL2 controls glucocorticoid-induced apoptosis of pediatric acute lymphoblastic leukemia cells. Jing D, Bhadri VA, Beck D, Thoms JA, Yakob NA, Wong JW, Knezevic K, Pimanda JE, Lock RB. , PMID:25336632
MINSEQE
Exp. designProtocolsVariablesProcessedSeq. reads
Files
Investigation descriptionE-GEOD-58266.idf.txt
Sample and data relationshipE-GEOD-58266.sdrf.txt
Processed data (2)E-GEOD-58266.processed.1.zip, E-GEOD-58266.processed.2.zip
Links