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dc.contributor.authorWorkman, Pen_US
dc.date.accessioned2018-06-25T15:26:26Z
dc.date.issued2004-04en_US
dc.identifier.citationBiochemical Society transactions, 2004, 32 (Pt 2), pp. 393 - 396en_US
dc.identifier.issn0300-5127en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1919
dc.identifier.eissn1470-8752en_US
dc.identifier.doi10.1042/bst0320393en_US
dc.description.abstractThere is extensive evidence from the molecular and genomic analysis of human cancers that the PI 3-kinase (phosphoinositide 3-kinase)-Akt/PKB (protein kinase B) pathway is deregulated in malignant progression. Furthermore, the causal involvement of PI 3-kinase is supported by gene-knockout mouse models. Prototype inhibitors show evidence of anticancer activity in vitro and in vivo animal models. The recent development of isoform-selective inhibitors shows considerable promise for cancer treatment.en_US
dc.formatPrinten_US
dc.format.extent393 - 396en_US
dc.languageengen_US
dc.language.isoengen_US
dc.subjectAnimalsen_US
dc.subjectMice, Knockouten_US
dc.subjectHumansen_US
dc.subjectMiceen_US
dc.subjectNeoplasmsen_US
dc.subjectDisease Models, Animalen_US
dc.subjectDisease Progressionen_US
dc.subjectProtein Isoformsen_US
dc.subjectAntineoplastic Agentsen_US
dc.subjectEnzyme Inhibitorsen_US
dc.subjectGenomeen_US
dc.subjectModels, Chemicalen_US
dc.subjectPhosphatidylinositol 3-Kinasesen_US
dc.titleInhibiting the phosphoinositide 3-kinase pathway for cancer treatment.en_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1042/bst0320393en_US
rioxxterms.licenseref.startdate2004-04en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfBiochemical Society transactionsen_US
pubs.issuePt 2en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.publication-statusPublisheden_US
pubs.volume32en_US
pubs.embargo.termsNot knownen_US
dc.contributor.icrauthorWorkman, Paulen_US


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