Faithful DNA Replication Requires Regulation of CDK Activity by Checkpoint Kinases

Sørensen, Claus Storgaard; Beck, Halfdan; Syljuåsen, Randi G.

doi:10.5772/18616

Cited by 1 publication

(2 citation statements)

References 140 publications

(119 reference statements)

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“…In response to replication damage and stress, ataxia telangiectasia and Rad3-related protein kinase (ATR) and cycle checkpoint kinase 1 (CHK1) activate the S phase checkpoint (Nam & Cortez 2011, Zeman & Cimprich 2014, which slows down replication forks and prevents replication origin firing (Figure 4) (Cliby et al 1998, Friedel et al 2009, Seiler et al 2007). The S phase checkpoint promotes DNA repair and prevents premature mitosis, thereby maintaining genomic stability (Nam & Cortez 2011, Zeman & Cimprich 2014 Karnitz & Zou 2015, Seiler et al 2007, Sørensen et al 2011. Consistently, combinations of ATR or CHK1 inhibitors with PARPis show synergistic effects (Murai et al 2016, Tang et al 2012).…”

Section: Cell Cycle Checkpoint Genesmentioning

confidence: 94%

“…The highly synergistic effects of PARPis in combination with alkylating agents (TMZ and MMS) and TOP1 inhibitors (camptothecins and indenoisoquinolines) are well documented (Davidson et al 2013, Shelton et al 2013, Tahara et al 2014, Tentori et al 2006. Both alkylating agents and TOP1 inhibitors induce DNA SSBs sensed by PARP1.…”

Section: Rationale For Combinations Of Parpis With Dna-damaging Agents In Relationship With Parp Trappingmentioning

confidence: 99%

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PARP Trapping Beyond Homologous Recombination and Platinum Sensitivity in Cancers

Murai

Pommier

2019

Annu. Rev. Cancer Biol.

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Poly(ADP-ribose) polymerase inhibitors (PARPis) have recently been approved for the treatment of ovarian and breast cancers with BRCA mutations, as well as for maintenance therapies regardless of BRCA mutation for ovarian and primary peritoneal cancers that previously responded to platinum-based chemotherapy. The rationale of these indications is derived from the facts that cancer cells with BRCA mutations are defective in homologous recombination (HR), which confers synthetic lethality with PARPis, and that some of the sensitivity-determining factors for PARPis are shared with platinums. Although BRCA1 and BRCA2 are central for HR, more players within and beyond HR are emerging as response determinants to PARPis. Furthermore, there are similarities as well as differences in the DNA lesions and repair pathways induced by PARPis, platinums, and camptothecin topoisomerase 1 (TOP1) inhibitors. Here we review the sensitivity-determining factors for PARPis and the rationale for using PARPis as single agents and in combination therapy for cancers.

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Section: Cell Cycle Checkpoint Genesmentioning

confidence: 94%

Section: Rationale For Combinations Of Parpis With Dna-damaging Agents In Relationship With Parp Trappingmentioning

confidence: 99%

PARP Trapping Beyond Homologous Recombination and Platinum Sensitivity in Cancers

Murai

Pommier

2019

Annu. Rev. Cancer Biol.

View full text Add to dashboard Cite

show abstract

Faithful DNA Replication Requires Regulation of CDK Activity by Checkpoint Kinases

Cited by 1 publication

References 140 publications

PARP Trapping Beyond Homologous Recombination and Platinum Sensitivity in Cancers

PARP Trapping Beyond Homologous Recombination and Platinum Sensitivity in Cancers

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