Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy

被引:1827
作者
Fulda, S. [1 ]
Debatin, K. -M [1 ]
机构
[1] Univ Ulm, Childrens Hosp, D-89075 Ulm, Germany
关键词
apoptosis; death receptor; mitochondria; cancer; chemotherapy;
D O I
10.1038/sj.onc.1209608
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
Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.
引用
收藏
页码:4798 / 4811
页数:14
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