Cancer results from a disordered and unstable genome - the degree of abnormality progresses as the process of oncogenesis proceeds. Such genomic instability appears to be subject to control by environmental factors as evidenced by the number of cancers that are either caused by specific environmental agents (lung, skin, cervix) or else regulated by a broader range of agents such as effect of diet on gastric and colorectal cancers. Dietary factors might interact in several ways with the genome to protect against cancer. An agent might interact directly with the genome and regulate expression (as a genetic or epigenetic regulator) or indirectly by influencing DNA 'repair' responses and so improve genomic stability. Research now shows that diet-genomic interactions in cancer go beyond interactions with the normal genome and involve enhancement of normal cellular responses to DNA damage such that genome stability is more effectively maintained. Activation of apoptosis may be a key to protection.