Interference of glucocorticoids with apoptosis signaling and host-tumor interactions

被引:45
作者
Rutz, HP [1 ]
Herr, I
机构
[1] Paul Scherrer Inst, Div Radiat Med, CH-5232 Villigen, Switzerland
[2] German Canc Res Ctr, DKFZ, Mol Oncol Pediat Unit, D-6900 Heidelberg, Germany
关键词
cancer; dexamethasone; prednisone; radiation therapy; chemotherapy; resistance failure; cachexia;
D O I
10.4161/cbt.3.8.966
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The cure of cancer is compromised by a variety of factors and mechanisms, which include tissue origin of the malignant cells, tumor load and hypoxia, impediment of drug access, and cellular resistance to treatment. Treatment resistance may be intrinsic, acquired, or induced, and it may occur to either radiation or a single drug alone, or simultaneously to multiple agents. Although the problem of corticosteroid-induced and hence, iatrogenic resistance to the treatment of cancer has continuously gained some interest over the past several years, no measures have been taken yet to diligently examine this problem in the clinical situation. In this review, we address several additional mechanisms through which glucocorticoids may influence the result of cytotoxic therapy of cancer, like: inducible interference with apoptosis signaling; interference with immune response against malignant cells; issues relating to their impact on glucose metabolism in cancer patients.
引用
收藏
页码:715 / 718
页数:4
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