Journal
JOURNAL OF CLINICAL ONCOLOGY
Volume 26, Issue 22, Pages 3785-3790Publisher
AMER SOC CLINICAL ONCOLOGY
DOI: 10.1200/JCO.2008.16.0812
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Funding
- Cancer Research UK [A8363] Funding Source: Medline
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Cancer cells frequently harbor defects in DNA repair pathways, leading to genomic instability. This can foster tumorigenesis but also provides a weakness in the tumor that can be exploited therapeutically. Tumors with compromised ability to repair double-strand DNA breaks by homologous recombination, including those with defects in BRCA1 and BRCA2, are highly sensitive to blockade of the repair of DNA single-strand breaks via the inhibition of the enzyme poly(ADP) ribose polymerase. This provides the basis for a novel synthetic lethal approach to cancer therapy.
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