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dc.contributor.authorBaxter, JS
dc.contributor.authorZatreanu, D
dc.contributor.authorPettitt, SJ
dc.contributor.authorLord, CJ
dc.coverage.spatialUnited States
dc.date.accessioned2022-07-19T10:23:42Z
dc.date.available2022-07-19T10:23:42Z
dc.date.issued2022-05-14
dc.identifier.citationMolecular Oncology, 2022,en_US
dc.identifier.issn1574-7891
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/5244
dc.identifier.eissn1878-0261
dc.identifier.eissn1878-0261
dc.identifier.doi10.1002/1878-0261.13224
dc.identifier.doi10.1002/1878-0261.13224
dc.description.abstractThe DNA damage response (DDR) represents a complex network of proteins which detect and repair DNA damage, thereby maintaining the integrity of the genome and preventing the transmission of mutations and rearranged chromosomes to daughter cells. Faults in the DDR are a known driver and hallmark of cancer. Furthermore, inhibition of DDR enzymes can be used to treat the disease. This is exemplified by PARP inhibitors (PARPi) used to treat cancers with defects in the homologous recombination DDR pathway. A series of novel DDR targets are now also under pre-clinical or clinical investigation, including inhibitors of ATR kinase, WRN helicase or the DNA polymerase/helicase Polθ (Pol-Theta). Drug resistance is a common phenomenon that impairs the overall effectiveness of cancer treatments and there is already some understanding of how resistance to PARPi occurs. Here, we discuss how an understanding of PARPi resistance could inform how resistance to new drugs targeting the DDR emerges. We also discuss potential strategies that could limit the impact of these therapy resistance mechanisms in cancer.
dc.formatPrint-Electronic
dc.languageeng
dc.language.isoengen_US
dc.publisherWILEYen_US
dc.relation.ispartofMolecular Oncology
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectATR
dc.subjectCancer
dc.subjectDDR
dc.subjectPARP
dc.subjectPolQ
dc.subjectWRN
dc.titleResistance to DNA repair inhibitors in cancer.en_US
dc.typeJournal Article
dcterms.dateAccepted2022-05-12
dc.date.updated2022-07-19T10:23:14Z
rioxxterms.versionVoRen_US
rioxxterms.versionofrecord10.1002/1878-0261.13224en_US
rioxxterms.licenseref.startdate2022-05-14
rioxxterms.typeJournal Article/Reviewen_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/35567571
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function
pubs.publication-statusPublished online
icr.researchteamGene Functionen_US
dc.contributor.icrauthorLord, Christopher
icr.provenanceDeposited by Mr Arek Surman on 2022-07-19. Deposit type is initial. No. of files: 1. Files: Molecular Oncology - 2022 - Baxter - Resistance to DNA repair inhibitors in cancer.pdf


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