Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

Hannah Farmer, Nuala McCabe, Christopher J. Lord, Andrew N. J. Tutt, Damian A. Johnson, Tobias B. Richardson, Manuela Santarosa, Krystyna J. Dillon, Ian Hickson, Charlotte Knights, Niall M. B. Martin, Stephen P. Jackson, Graeme C. M. Smith () and Alan Ashworth ()
Additional contact information
Hannah Farmer: Cancer Research UK Gene Function and Regulation Group
Nuala McCabe: Cancer Research UK Gene Function and Regulation Group
Christopher J. Lord: The Breakthrough Breast Cancer Research Centre Institute of Cancer Research
Andrew N. J. Tutt: The Breakthrough Breast Cancer Research Centre Institute of Cancer Research
Damian A. Johnson: The Breakthrough Breast Cancer Research Centre Institute of Cancer Research
Tobias B. Richardson: The Breakthrough Breast Cancer Research Centre Institute of Cancer Research
Manuela Santarosa: The Breakthrough Breast Cancer Research Centre Institute of Cancer Research
Krystyna J. Dillon: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Ian Hickson: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Charlotte Knights: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Niall M. B. Martin: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Stephen P. Jackson: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Graeme C. M. Smith: KuDOS Pharmaceuticals Ltd, Cambridge Science Park
Alan Ashworth: Cancer Research UK Gene Function and Regulation Group

Nature, 2005, vol. 434, issue 7035, 917-921

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/nature03445

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