From Breaking Bad to Worse: Exploiting Homologous DNA Repair Deficiency in Cancer
Name
Hemann_From breaking.pdf
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84.29 KB
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Author(s)
Hemann, Michael
Date Issued
May 2014
Journal
Cancer Discovery
Publisher
American Association for Cancer Research
Citation
Hemann, M. T. “From Breaking Bad to Worse: Exploiting Homologous DNA Repair Deficiency in Cancer.” Cancer Discovery 4, no. 5 (May 1, 2014): 516–518.
Version
Author's final manuscript
Abstract
DNA repair deficiencies are common among cancer cells and represent a potential vulnerability that might be exploited by targeting compensatory repair pathways. However, the identification of synthetically lethal combinations of DNA repair defects, although of significant clinical relevance, has been somewhat anecdotal. Although numerous models have been proposed to explain synthetic lethality among DNA repair mutations, we have only a limited understanding of why a given mutation should render cells sensitive to another. In this issue of Cancer Discovery, Dietlein and colleagues define a general connection between mutations in genes involved in homologous recombination and sensitivity to inhibitors of non-homologous end joining. In doing so, they provide a mechanism to demarcate a set of seemingly diverse tumors that may be highly responsive to established DNA repair–targeted therapeutics.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
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Creative Commons Attribution-Noncommercial-Share Alike
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DOI of Published Version
https://doi.org/10.1158/2159-8290.cd-14-0316
