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


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-04

AUTHORS

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, Alan Ashworth

ABSTRACT

BRCA1 and BRCA2 are important for DNA double-strand break repair by homologous recombination, and mutations in these genes predispose to breast and other cancers. Poly(ADP-ribose) polymerase (PARP) is an enzyme involved in base excision repair, a key pathway in the repair of DNA single-strand breaks. We show here that BRCA1 or BRCA2 dysfunction unexpectedly and profoundly sensitizes cells to the inhibition of PARP enzymatic activity, resulting in chromosomal instability, cell cycle arrest and subsequent apoptosis. This seems to be because the inhibition of PARP leads to the persistence of DNA lesions normally repaired by homologous recombination. These results illustrate how different pathways cooperate to repair damage, and suggest that the targeted inhibition of particular DNA repair pathways may allow the design of specific and less toxic therapies for cancer. More... »

PAGES

917

Journal

TITLE

Nature

ISSUE

7035

VOLUME

434

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature03445

    DOI

    http://dx.doi.org/10.1038/nature03445

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1039649759

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15829967


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