Nonhomologous end joining is essential for cellular resistance to the novel antitumor agent, beta-lapachone.

@article{Bentle2007NonhomologousEJ,
  title={Nonhomologous end joining is essential for cellular resistance to the novel antitumor agent, beta-lapachone.},
  author={Melissa S. Bentle and Kathryn E. Reinicke and Ying Dong and Erik A. Bey and David A. Boothman},
  journal={Cancer research},
  year={2007},
  volume={67 14},
  pages={6936-45}
}
Commonly used antitumor agents, such as DNA topoisomerase I/II poisons, kill cancer cells by creating nonrepairable DNA double-strand breaks (DSBs). To repair DSBs, error-free homologous recombination (HR), and/or error-prone nonhomologous end joining (NHEJ) are activated. These processes involve the phosphatidylinositol 3'-kinase-related kinase family of serine/threonine enzymes: ataxia telangiectasia mutated (ATM), ATM- and Rad3-related for HR, and DNA-dependent protein kinase catalytic… CONTINUE READING

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