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Cancers arise through the acquisition of oncogenic mutations and grow through clonal expansion 1,2. Here we reveal that most mutagenic DNA lesions are not resolved as mutations within a single cell-cycle. Instead, DNA lesions segregate unrepaired into daughter cells for multiple cell generations, resulting in the chromosome-scale phasing of subsequent mutations. We characterise this process in mutagen-induced mouse liver tumours and show that DNA replication across persisting lesions candoi:10.1101/868679 fatcat:43cdxjkqnfcjjpwnenqwws5mk4