The DNA damage response (DDR) and the replication stress response (RSR) represent highly conserved pathways that cooperate to prevent accumulation of DNA lesions and thereby guard cells against genomic instability.
The DNA damage response (DDR) and the replication stress response (RSR) represent highly conserved pathways that cooperate to prevent accumulation of DNA lesionsand thereby guard cells against genomic instability. Both pathways are frequently deregulated in human cancers, allowing cancer cells to acquire mutations at significantly increased rates. While such defects in genome maintenance mechanisms promote cancer development, they can also provide a therapeutic opportunity if we can identify the specific vulnerabilities theyentail