Science
Cancer cells often exhibit chronic replication stress due to functional alterations of proteins that protect or repair DNA or are involved in control of transcriptional of replicative processes. Due to the continuous proliferative signaling in such tumor cells, enhancing replicative stress cells provides an exploitable therapeutic vulnerability (Reviewed, e.g., in Ubhi and Brown, Cancer Research 2019).
Novel agents which increase the existing deficiencies in cell-cycle, transcription and replication control in tumor cells are expected to enhance 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.