Literature DB >> 19755856

Exploiting synthetic lethal interactions for targeted cancer therapy.

H Christian Reinhardt1, Hai Jiang, Michael T Hemann, Michael B Yaffe.   

Abstract

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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Year:  2009        PMID: 19755856      PMCID: PMC3057180          DOI: 10.4161/cc.8.19.9626

Source DB:  PubMed          Journal:  Cell Cycle        ISSN: 1551-4005            Impact factor:   4.534


  93 in total

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10.  Ionizing radiation-induced Rad51 nuclear focus formation is cell cycle-regulated and defective in both ATM(-/-) and c-Abl(-/-) cells.

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  48 in total

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10.  A reversible gene-targeting strategy identifies synthetic lethal interactions between MK2 and p53 in the DNA damage response in vivo.

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