4.6 Article

Exploiting synthetic lethal interactions for targeted cancer therapy

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

资金

  1. NIH [GM68762, CA112967, ES015339]
  2. NIH Integrative Cancer Biology Program [U54-CA112967-03]
  3. Deutsche Forschungsgemeinschaft [RE2246/1-1]
  4. Deutsche Nierenstiftung
  5. David H. Koch Fund

向作者/读者索取更多资源

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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