Figure 5.

Proposed model of the molecular and cellular responses to new replication stress inhibitors. ATR/CHK1 stabilizes replication forks and prevents their collapse into DSBs. SSBs can be accurately repaired using the undamaged strand as a template, a process involving the PARP enzyme. SSBs are mainly repaired through the homologous recombination (HR) pathway. BRCA is related to the error-free repair of DSBs by HR. ATRi or CHK1i in monotherapy and in combined treatment with PARPi cause genome instability and leads to the synthetic lethality of ovarian cancer cells.