Glucocorticoid resistance in paediatric acute lymphoblastic leukaemia

被引：45

作者：

Bhadri, Vivek A. ^{[1
,2
]}

Trahair, Toby N. ^{[2
]}

Lock, Richard B.

机构：

[1] Univ New S Wales, Lowy Canc Res Ctr, Childrens Canc Inst Australia Med Res, Randwick, NSW 2031, Australia

[2] Univ New S Wales, Sydney Childrens Hosp, Ctr Childrens Canc & Blood Disorders, Randwick, NSW 2031, Australia

来源：

JOURNAL OF PAEDIATRICS AND CHILD HEALTH | 2012年 / 48卷 / 08期

基金：

英国医学研究理事会;

关键词：

glucocorticoid; haematology; leukaemia; oncology; GAMMA-SECRETASE INHIBITORS; MESSENGER-RNA EXPRESSION; INDUCED APOPTOSIS; BH3-ONLY PROTEINS; CELL-DEATH; RECEPTOR-ALPHA; CHILDHOOD; THERAPY; GENE; DEXAMETHASONE;

D O I：

10.1111/j.1440-1754.2011.02212.x

中图分类号：

R72 [儿科学];

学科分类号：

100202 ;

摘要：

Glucocorticoids (GCs), such as prednisolone and dexamethasone, are key components in multi-agent chemotherapy protocols used for the treatment of acute lymphoblastic leukaemia (ALL). Approximately 10% of children with ALL will respond poorly to GCs, and GC resistance is associated with a significantly inferior outcome. This review summarises the current knowledge of GC resistance in ALL, including the roles of the GC receptor and its co-chaperone molecules, the pro-apoptotic and pro-survival B-cell lymphoma 2 family members and alternative non-apoptotic mechanisms of cell death. It concludes with a discussion on therapeutic attempts to overcome GC resistance.

引用

页码：634 / 640

页数：7

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