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dc.contributor.authorBrandsma, I
dc.contributor.authorFleuren, EDG
dc.contributor.authorWilliamson, CT
dc.contributor.authorLord, CJ
dc.date.accessioned2018-02-14T10:50:33Z
dc.date.issued2017-12
dc.identifier.citationExpert opinion on investigational drugs, 2017, 26 (12), pp. 1341 - 1355
dc.identifier.issn1354-3784
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1071
dc.identifier.eissn1744-7658
dc.identifier.doi10.1080/13543784.2017.1389895
dc.description.abstractIntroduction Defects in the DNA damage response (DDR) drive the development of cancer by fostering DNA mutation but also provide cancer-specific vulnerabilities that can be exploited therapeutically. The recent approval of three different PARP inhibitors for the treatment of ovarian cancer provides the impetus for further developing targeted inhibitors of many of the kinases involved in the DDR, including inhibitors of ATR, ATM, CHEK1, CHEK2, DNAPK and WEE1. Areas covered: We summarise the current stage of development of these novel DDR kinase inhibitors, and describe which predictive biomarkers might be exploited to direct their clinical use. Expert opinion: Novel DDR inhibitors present promising candidates in cancer treatment and have the potential to elicit synthetic lethal effects. In order to fully exploit their potential and maximize their utility, identifying highly penetrant predictive biomarkers of single agent and combinatorial DDR inhibitor sensitivity are critical. Identifying the optimal drug combination regimens that could used with DDR inhibitors is also a key objective.
dc.formatPrint-Electronic
dc.format.extent1341 - 1355
dc.languageeng
dc.language.isoeng
dc.subjectAnimals
dc.subjectHumans
dc.subjectNeoplasms
dc.subjectDNA Damage
dc.subjectAntineoplastic Agents
dc.subjectProtein Kinase Inhibitors
dc.subjectDrug Design
dc.subjectMutation
dc.subjectMolecular Targeted Therapy
dc.subjectBiomarkers
dc.subjectPoly(ADP-ribose) Polymerase Inhibitors
dc.titleDirecting the use of DDR kinase inhibitors in cancer treatment.
dc.typeJournal Article
dcterms.dateAccepted2017-10-04
rioxxterms.versionofrecord10.1080/13543784.2017.1389895
rioxxterms.licenseref.startdate2017-12
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfExpert opinion on investigational drugs
pubs.issue12
pubs.notesNot known
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.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
pubs.volume26
pubs.embargo.termsNot known
icr.researchteamGene Functionen_US
dc.contributor.icrauthorLord, Christopheren


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