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dc.contributor.authorRafii, S
dc.contributor.authorGourley, C
dc.contributor.authorKumar, R
dc.contributor.authorGeuna, E
dc.contributor.authorErn Ang, J
dc.contributor.authorRye, T
dc.contributor.authorChen, L-M
dc.contributor.authorShapira-Frommer, R
dc.contributor.authorFriedlander, M
dc.contributor.authorMatulonis, U
dc.contributor.authorDe Greve, J
dc.contributor.authorOza, AM
dc.contributor.authorBanerjee, S
dc.contributor.authorMolife, LR
dc.contributor.authorGore, ME
dc.contributor.authorKaye, SB
dc.contributor.authorYap, TA
dc.date.accessioned2017-05-26T15:37:33Z
dc.date.issued2017-07
dc.identifier.citationOncotarget, 2017, 8 (29), pp. 47154 - 47160
dc.identifier.issn1949-2553
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/665
dc.identifier.eissn1949-2553
dc.identifier.doi10.18632/oncotarget.17005
dc.description.abstractBackground The PARP inhibitor olaparib was recently granted Food and Drug Administration (FDA) accelerated approval in patients with advanced BRCA1/2 mutation ovarian cancer. However, antitumor responses are observed in only approximately 40% of patients and the impact of baseline clinical factors on response to treatment remains unclear. Although platinum sensitivity has been suggested as a marker of response to PARP inhibitors, patients with platinum-resistant disease still respond to olaparib.Results 108 patients with advanced BRCA1/2 mutation ovarian cancers were included. The interval between the end of the most recent platinum chemotherapy and PARPi (PTPI) was used to predict response to olaparib independent of conventional definition of platinum sensitivity. RECIST complete response (CR) and partial response (PR) rates were 35% in patients with platinum-sensitive versus 13% in platinum-resistant (p<0.005). Independent of platinum sensitivity status, the RECIST CR/PR rates were 42% in patients with PTPI greater than 52 weeks and 18% in patients with PTPI less than 52 weeks (p=0.016). No association was found between baseline clinical factors such as FIGO staging, debulking surgery, BRCA1 versus BRCA2 mutations, prior history of breast cancer and prior chemotherapy for breast cancer, and the response to olaparib.Methods We conducted an international multicenter retrospective study to investigate the association between baseline clinical characteristics of patients with advanced BRCA1/2 mutation ovarian cancers from eight different cancer centers and their antitumor response to olaparib.Conclusion PTPI may be used to refine the prediction of response to PARP inhibition based on the conventional categorization of platinum sensitivity.
dc.formatPrint
dc.format.extent47154 - 47160
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectHumans
dc.subjectOvarian Neoplasms
dc.subjectNeoplasm Metastasis
dc.subjectRecurrence
dc.subjectPiperazines
dc.subjectPhthalazines
dc.subjectBRCA1 Protein
dc.subjectBRCA2 Protein
dc.subjectAntineoplastic Agents
dc.subjectNeoplasm Staging
dc.subjectPrognosis
dc.subjectTreatment Outcome
dc.subjectSurvival Analysis
dc.subjectGerm-Line Mutation
dc.subjectAdult
dc.subjectAged
dc.subjectMiddle Aged
dc.subjectFemale
dc.subjectNeoplasm Grading
dc.subjectPoly(ADP-ribose) Polymerase Inhibitors
dc.titleBaseline clinical predictors of antitumor response to the PARP inhibitor olaparib in germline BRCA1/2 mutated patients with advanced ovarian cancer.
dc.typeJournal Article
dcterms.dateAccepted2017-02-22
rioxxterms.versionofrecord10.18632/oncotarget.17005
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2017-07
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfOncotarget
pubs.issue29
pubs.notesNo embargo
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/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Medicine Drug Development Unit (de Bono)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Medicine Drug Development Unit (de Bono)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Medicine Drug Development Unit (Kaye)
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
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/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Medicine Drug Development Unit (de Bono)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Medicine Drug Development Unit (de Bono)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Medicine Drug Development Unit (Kaye)
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.publication-statusPublished
pubs.volume8
pubs.embargo.termsNo embargo
icr.researchteamMedicine Drug Development Unit (de Bono)en_US
icr.researchteamMedicine Drug Development Unit (Kaye)en_US
dc.contributor.icrauthorYap, Timothyen
dc.contributor.icrauthorGore, Martinen
dc.contributor.icrauthorBanerjee, Susanaen
dc.contributor.icrauthorMolife, Rhodaen
dc.contributor.icrauthorMarsden,en
dc.contributor.icrauthorKaye, Stanley Bernarden


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