LYMPHOID NEOPLASIA Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition
نویسندگان
چکیده
1Children’s Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, University of New South Wales, Sydney, Australia; 2Department of Clinical Medicine, University of Milano-Bicocca, Monza, Italy; 3Lowy Cancer Research Centre and the Prince of Wales Clinical School, University of New South Wales, Sydney, Australia; 4Murdoch Childrens Research Institute, Royal Children’s Hospital, Department of Paediatrics, The University of Melbourne, Parkville, Australia; 5Centre for Children’s Cancer and Blood Disorders, Sydney Children’s Hospital, Randwick, Australia; 6Centro Ricerca clinica Tettamanti, Clinica Pediatrica, University of Milano-Bicocca, Monza, Italy; and 7Cambridge Institute for Medical Research, University of Cambridge, Cambridge, United Kingdom
منابع مشابه
Epigenetic silencing of BIM in glucocorticoid poor-responsive pediatric acute lymphoblastic leukemia, and its reversal by histone deacetylase inhibition.
Glucocorticoids play a critical role in the therapy of lymphoid malignancies, including pediatric acute lymphoblastic leukemia (ALL), although the mechanisms underlying cellular resistance remain unclear. We report glucocorticoid resistance attributable to epigenetic silencing of the BIM gene in pediatric ALL biopsies and xenografts established in immune-deficient mice from direct patient expla...
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Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). The proapoptotic BIM protein is an important mediator of glucocorticoid-induced apoptosis in normal and malignant lymphocytes, whereas the antiapoptotic BCL2 confers resistance. The signaling pathways regulating BIM and BCL2 expression in glucocorticoid-treated lymphoid ...
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