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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

Released on 18 December 2014, last updated on 2 January 2015
Homo sapiens
Samples (6)
Protocols (1)
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
Dominik Beck, Duohui Jing, Jason W Wong, John E Pimanda, Richard B Lock
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
Exp. designProtocolsVariablesProcessedSeq. reads
Investigation descriptionE-GEOD-58266.idf.txt
Sample and data relationshipE-GEOD-58266.sdrf.txt
Processed data (2),