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Challenging this assumption are recent findings that indicate chemotherapies such as cisplatin used to treat BRCA-deficient tumors do not initially cause DNA double-strand-breaks (DSB). Here we show that single-stranded DNA (ssDNA) replication gaps underlie the hypersensitivity of BRCA-deficient cancer and that defects in homologous recombination (HR) or fork protection (FP) do not. In BRCA-deficient cells, ssDNA gaps developed because replication was not effectively restrained in response todoi:10.1158/0008-5472.can-20-1602 pmid:33184108 fatcat:sjvzish3wzdxfah5yxb4ijt3gy