期刊
CELL DEATH AND DIFFERENTIATION
卷 25, 期 1, 页码 27-36出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2017.161
关键词
-
资金
- National Health and Medical Research Council [461221, 1016701, 1016647, 1079560, 1041797]
- SCOR grants from the Leukemia & Lymphoma Society [7001-15]
- Victorian Cancer Agency
- Cancer Council Victoria
- Australian Cancer Research Foundation
- government of Australia (IRIISS) [9000220]
- government of Victoria (OIS grant)
Impaired apoptosis plays a central role in cancer development and limits the efficacy of conventional cytotoxic therapies. Deepening understanding of how opposing factions of the BCL-2 protein family switch on apoptosis and of their structures has driven development of a new class of cancer drugs that targets various pro-survival members by mimicking their natural inhibitors, the BH3-only proteins. These 'BH3 mimetic' drugs seem destined to become powerful new weapons in the arsenal against cancer. Successful clinical trials of venetoclax/ABT-199, a specific inhibitor of BCL-2, have led to its approval for a refractory form of chronic lymphocytic leukaemia and to scores of on-going trials for other malignancies. Furthermore, encouraging preclinical studies of BH3 mimetics that target other BCL-2 pro-survival members, particularly MCL-1, offer promise for cancers resistant to venetoclax. This review sketches the impact of the BCL-2 family on cancer development and therapy, describes how interactions of family members trigger apoptosis and discusses the potential of BH3 mimetic drugs to advance cancer therapy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据