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BRCA mutations cause tumor cells to lose the ability to repair double-strand DNA breaks by homologous recombination. However, this loss of function can be compensated for in such cancer cells by base-excision repair, which is mediated by the enzyme poly(adenosine diphosphate ribose) polymerase (PARP). Would inhibiting PARP be an effective cancer treatment in BRCA-mutation carriers?
To test this strategy, investigators in the U.K. and the Netherlands conducted an industry-supported, phase I trial of the oral PARP inhibitor olaparib. The trial involved 60 patients (with melanomas or breast, ovarian, prostate, or colorectal tumors), 23 of whom carried BRCA1 or BRCA2 mutations. All patients had previously received ≥1 treatment regimen; most (53%…