Apoptosis defects and chemotherapy resistance: molecular interaction maps and networks

被引:481
作者
Pommier, Y
Sordet, O
Antony, S
Hayward, RL
Kohn, KW
机构
[1] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH,DHHS, Bethesda, MD 20892 USA
[2] Western Gen Hosp, Canc Res United Kingdom, Edinburgh EH4 2XU, Midlothian, Scotland
关键词
cancer chemotherapy; apoptosis; multidrug resistance; camptothecins;
D O I
10.1038/sj.onc.1207515
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Intrinsic (innate) and acquired (adaptive) resistance to chemotherapy critically limits the outcome of cancer treatments. For many years, it was assumed that the interaction of a drug with its molecular target would yield a lethal lesion, and that determinants of intrinsic drug resistance should therefore be sought either at the target level (quantitative changes or/and mutations) or upstream of this interaction, in drug metabolism or drug transport mechanisms. It is now apparent that independent of the factors above, cellular responses to a molecular lesion can determine the outcome of therapy. This review will focus on programmed cell death (apoptosis) and on survival pathways (Bcl-2, Apaf-1, AKT, NF-kappaB) involved in multidrug resistance. We will present our molecular interaction mapping conventions to summarize the AKT and IkappaB/NF-kappaB networks. They complement the p53, Chk2 and c-Abl maps published recently. We will also introduce the 'permissive apoptosis-resistance' model for the selection of multidrug-resistant cells.
引用
收藏
页码:2934 / 2949
页数:16
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