Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

Helen E. Bryant, Niklas Schultz, Huw D. Thomas, Kayan M. Parker, Dan Flower, Elena Lopez, Suzanne Kyle, Mark Meuth, Nicola J. Curtin and Thomas Helleday ()
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Helen E. Bryant: University of Sheffield, Medical School
Niklas Schultz: Microbiology and Toxicology, Arrhenius Laboratory, Stockholm University
Huw D. Thomas: University of Newcastle upon Tyne, Medical School
Kayan M. Parker: University of Sheffield, Medical School
Dan Flower: University of Sheffield, Medical School
Elena Lopez: University of Sheffield, Medical School
Suzanne Kyle: University of Newcastle upon Tyne, Medical School
Mark Meuth: University of Sheffield, Medical School
Nicola J. Curtin: University of Newcastle upon Tyne, Medical School
Thomas Helleday: University of Sheffield, Medical School

Nature, 2005, vol. 434, issue 7035, 913-917

Abstract: Cancer therapy: stop PARP The discovery that BRCA1/2 mutant cells (defective in the homologous recombination pathway of DNA repair) are spectacularly sensitive to inhibition of the enzyme PARP (involved in base excision repair) suggests a new, low toxicity, approach to the treatment of women with breast cancers caused by BRCA mutations. As the PARP inhibitors have no effect on cells with functional homologous recombination, the hope is that the treatment will be specific for breast cancer cells. PARP-inhibiting chemotherapeutics may be able to make use of a ‘synthetic lethal’ effect as an alternative to conventional nonspecific cytotoxic anticancer treatments.

Date: 2005
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DOI: 10.1038/nature03443

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