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dc.contributor.authorBrown, JS
dc.contributor.authorBanerji, U
dc.date.accessioned2017-02-01T12:23:33Z
dc.date.issued2017-04-01
dc.identifier.citationPharmacology & therapeutics, 2017, 172 pp. 101 - 115
dc.identifier.issn0163-7258
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/400
dc.identifier.eissn1879-016X
dc.identifier.doi10.1016/j.pharmthera.2016.12.001
dc.description.abstractPI3K/AKT signalling is commonly disrupted in human cancers, with AKT being a central component of the pathway, influencing multiple processes that are directly involved in tumourigenesis. Targeting AKT is therefore a highly attractive anti-cancer strategy with multiple AKT inhibitors now in various stages of clinical development. In this review, we summarise the role and regulation of AKT signalling in normal cellular physiology. We highlight the mechanisms by which AKT signalling can be hyperactivated in cancers and discuss the past, present and future clinical strategies for AKT inhibition in oncology.
dc.formatPrint-Electronic
dc.format.extent101 - 115
dc.languageeng
dc.language.isoeng
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectAnimals
dc.subjectHumans
dc.subjectNeoplasms
dc.subjectAntineoplastic Agents
dc.subjectProtein Kinase Inhibitors
dc.subjectSignal Transduction
dc.subjectDrug Design
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectPhosphatidylinositol 3-Kinase
dc.titleMaximising the potential of AKT inhibitors as anti-cancer treatments.
dc.typeJournal Article
dcterms.dateAccepted2016-11-16
rioxxterms.versionofrecord10.1016/j.pharmthera.2016.12.001
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2017-04
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfPharmacology & therapeutics
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/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/Clinical Pharmacology – Adaptive Therapy
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Medicine Drug Development Unit (de Bono)
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/Clinical Pharmacology – Adaptive Therapy
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Medicine Drug Development Unit (de Bono)
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.publication-statusPublished
pubs.volume172
pubs.embargo.termsNot known
icr.researchteamClinical Pharmacology – Adaptive Therapy
icr.researchteamMedicine Drug Development Unit (de Bono)
dc.contributor.icrauthorBanerji, Udai


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