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Abstract Although poly(ADP-ribose) polymerase inhibitors (PARPi) show promise for treating homologous recombination-deficient cancers, the observed PARPi hypersensitivity in additional genetic contexts expands their potential use in precision oncology. Yet, the DNA lesions driving PARPi-induced cytotoxicity remain poorly defined. Here we uncover distinct replication-fork lesions in specific genomic regions as key determinants of PARPi cytotoxicity.
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