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

Author

Listed:
  • Hannah Farmer

    (Cancer Research UK Gene Function and Regulation Group
    The Breakthrough Breast Cancer Research Centre Institute of Cancer Research)

  • Nuala McCabe

    (Cancer Research UK Gene Function and Regulation Group
    The Breakthrough Breast Cancer Research Centre Institute of Cancer Research)

  • 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
    Guy's Hospital)

  • 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
    CRO-IRCCS)

  • 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
    University of Cambridge)

  • Graeme C. M. Smith

    (KuDOS Pharmaceuticals Ltd, Cambridge Science Park)

  • Alan Ashworth

    (Cancer Research UK Gene Function and Regulation Group
    The Breakthrough Breast Cancer Research Centre Institute of Cancer Research)

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.

Suggested Citation

  • 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. , 2005. "Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy," Nature, Nature, vol. 434(7035), pages 917-921, April.
    • Handle: RePEc:nat:nature:v:434:y:2005:i:7035:d:10.1038_nature03445
    DOI: 10.1038/nature03445
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