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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Participation of the ATR/CHK1 pathway in replicative stress targeted therapy of high-grade ovarian cancer

Fig. 2

DNA damage and replication checkpoints. Anticancer drugs induce replication disorders. Replication stress is the effect of the slowing or stalling of replication fork progression. DNA synthesis inhibition or damage induces checkpoint responses controlled by the ATR–CHK1 pathway. DNA lesions delay entry to S-phase (G1 checkpoint), slow the replication of damaged DNA or prevent entry to mitosis (G2 checkpoint). Given that both PARP and checkpoint proteins prevent fork collapse, their corresponding inhibitors may increase the level of replication stress, genome instability and, in consequence, cell death

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