Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition.

@article{Mccabe2006DeficiencyIT,
  title={Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition.},
  author={N. Mccabe and Nicholas C. Turner and Christopher J. Lord and Katarzyna Kluzek and Aneta M Białkowska and Sally Swift and Sabrina Giavara and Mark J. O'Connor and Andrew N.J. Tutt and Malgorzata Z. Zdzienicka and Graeme C M Smith and Alan Ashworth},
  journal={Cancer research},
  year={2006},
  volume={66 16},
  pages={
          8109-15
        }
}
Deficiency in either of the breast cancer susceptibility proteins BRCA1 or BRCA2 induces profound cellular sensitivity to the inhibition of poly(ADP-ribose) polymerase (PARP) activity. We hypothesized that the critical role of BRCA1 and BRCA2 in the repair of double-strand breaks by homologous recombination (HR) was the underlying reason for this sensitivity. Here, we examine the effects of deficiency of several proteins involved in HR on sensitivity to PARP inhibition. We show that deficiency… Expand

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TLDR
It is shown that CAPAN-1 cells are in fact very sensitive to the potent PARP inhibitors KU0058684 (IC50 3.2nM) and K U0058948 (IC 50 3.4nM), and treatment with potent ParP inhibitors remains an exciting potential therapy for cancers involving BRCA1 or BRCa2 deficiency. Expand
Poly(ADP-ribose) polymerase (PARP-1) has a controlling role in homologous recombination.
TLDR
The data suggest that PARP-1 controls DNA damage recognised by HR and that it is not involved in executing HR as such. Expand
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