Cancer cells have evolved mechanisms to cope with replication stress, enabling their survival and proliferation despite the genomic instability. These mechanisms include:
Checkpoint activation: The ATR and Chk1 pathways are activated in response to replication stress, halting cell cycle progression to allow time for repair. DNA repair pathways: Enhanced DNA repair mechanisms, such as homologous recombination, help resolve replication-related DNA damage. Fork protection and stabilization: Proteins like BRCA1/2 and FANCD2 help stabilize and protect stalled replication forks from collapse.
