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dc.contributor.authorPascual, J
dc.contributor.authorTurner, NC
dc.date.accessioned2019-05-24T09:57:46Z
dc.date.issued2019-05-03
dc.identifier.citationAnnals of oncology : official journal of the European Society for Medical Oncology, 2019, 30 (7), pp. 1051 - 1060
dc.identifier.issn0923-7534
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3238
dc.identifier.eissn1569-8041
dc.identifier.doi10.1093/annonc/mdz133
dc.description.abstractTriple-negative breast cancer (TNBC) is characterised by poor outcomes and a historical lack of targeted therapies. Dysregulation of signalling through the phosphoinositide 3 (PI3)-kinase and AKT signalling pathway is one of the most frequent oncogenic aberrations of TNBC. Although mutations in individual genes occur relatively rarely, combined activating mutations in PIK3CA and AKT1, with inactivating mutations in phosphatase and tensin homologue, occur in ∼25%‒30% of advanced TNBC. Recent randomised trials suggest improved progression-free survival (PFS) with AKT-inhibitors in combination with first-line chemotherapy for patients with TNBC and pathway genetic aberrations. We review the evidence for PI3K pathway activation in TNBC, and clinical trial data for PI3K, AKT and mammalian target of rapamycin inhibitors in TNBC. We discuss uncertainty over defining which cancers have pathway activation and the future overlap between immunotherapy and pathway targeting.
dc.formatPrint
dc.format.extent1051 - 1060
dc.languageeng
dc.language.isoeng
dc.publisherOXFORD UNIV PRESS
dc.rights.urihttps://www.rioxx.net/licenses/under-embargo-all-rights-reserved
dc.subjectHumans
dc.subjectAntineoplastic Combined Chemotherapy Protocols
dc.subjectProtein Kinase Inhibitors
dc.subjectSignal Transduction
dc.subjectFemale
dc.subjectRandomized Controlled Trials as Topic
dc.subjectClinical Trials, Phase II as Topic
dc.subjectClinical Trials, Phase III as Topic
dc.subjectClass I Phosphatidylinositol 3-Kinases
dc.subjectMolecular Targeted Therapy
dc.subjectTriple Negative Breast Neoplasms
dc.titleTargeting the PI3-kinase pathway in triple-negative breast cancer.
dc.typeJournal Article
dcterms.dateAccepted2019-05-03
rioxxterms.versionofrecord10.1093/annonc/mdz133
rioxxterms.licenseref.urihttps://www.rioxx.net/licenses/under-embargo-all-rights-reserved
rioxxterms.licenseref.startdate2019-07
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfAnnals of oncology : official journal of the European Society for Medical Oncology
pubs.issue7
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/Molecular Oncology
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/Molecular Oncology
pubs.publication-statusPublished
pubs.volume30
pubs.embargo.termsNot known
icr.researchteamMolecular Oncology
dc.contributor.icrauthorPascual, Javier
dc.contributor.icrauthorTurner, Nicholas


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