期刊
CELL CYCLE
卷 8, 期 19, 页码 3112-3119出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.19.9626
关键词
DNA damage; signaling; cell cycle checkpoints; synthetic lethality; MAPKAP kinase-2; ATM; Chk2
类别
资金
- NIH [GM68762, CA112967, ES015339]
- NIH Integrative Cancer Biology Program [U54-CA112967-03]
- Deutsche Forschungsgemeinschaft [RE2246/1-1]
- Deutsche Nierenstiftung
- David H. Koch Fund
Emerging data suggests that synthetic lethal interactions between mutated oncogenes/tumor suppressor genes and molecules involved in DNA damage signaling and repair can be therapeutically exploited to preferentially kill tumor cells. In this review, we discuss the concept of synthetic lethality, and describe several recent examples in which this concept was successfully implemented to target tumor cells in culture, in mouse models, and in human cancer patients.
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