Science

Science

Cancer cells often exhibit chronic replication stress due to the loss of proteins that protect or repair DNA or are involved in cell-cycle control. Due to the continuous proliferative signaling in such tumor cells, targeting their DNA replication machinery provides an exploitable therapeutic vulnerability (Reviewed, e.g., in Ubhi and Brown, Cancer Research 2019).

Novel agents which enhance the existing deficiencies in cell-cycle checkpoint and DNA damage control in tumor cells are expected to increase the already inherent high basal level of replication stress in such cells, which stands in contrast to the low level of replicative stress present in normal “healthy” cells and tissues.