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dc.contributor.authorBroutin, Sen_US
dc.contributor.authorStewart, Aen_US
dc.contributor.authorThavasu, Pen_US
dc.contributor.authorPaci, Aen_US
dc.contributor.authorBidart, J-Men_US
dc.contributor.authorBanerji, Uen_US
dc.date.accessioned2016-08-26T14:25:24Z
dc.date.issued2016-08en_US
dc.identifier.citationBritish journal of cancer, 2016, 115 (5), pp. 549 - 552en_US
dc.identifier.issn0007-0920en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/73
dc.identifier.eissn1532-1827en_US
dc.identifier.doi10.1038/bjc.2016.220en_US
dc.description.abstractWe aimed to understand the dependence of MEK and m-TOR inhibition in EGFR(WT)/ALK(non-rearranged) NSCLC cell lines.In a panel of KRAS(M) and KRAS(WT) NSCLC cell lines, we determined growth inhibition (GI) following maximal reduction in p-ERK and p-S6RP caused by trametinib (MEK inhibitor) and AZD2014 (m-TOR inhibitor), respectively.GI caused by maximal m-TOR inhibition was significantly greater than GI caused by maximal MEK inhibition in the cell line panel (52% vs 18%, P<10(-4)). There was no significant difference in GI caused by maximal m-TOR compared with maximal m-TOR+MEK inhibition. However, GI caused by the combination was significantly greater in the KRAS(M) cell lines (79% vs 61%, P=0.017).m-TOR inhibition was more critical to GI than MEK inhibition in EGFR(WT)/ALK(non-rearranged) NSCLC cells. The combination of MEK and m-TOR inhibition was most effective in KRAS(M) cells.en_US
dc.formatPrint-Electronicen_US
dc.format.extent549 - 552en_US
dc.languageengen_US
dc.language.isoengen_US
dc.subjectCell Line, Tumoren_US
dc.subjectHumansen_US
dc.subjectCarcinoma, Non-Small-Cell Lungen_US
dc.subjectLung Neoplasmsen_US
dc.subjectMAP Kinase Kinase Kinasesen_US
dc.subjectSignal Transductionen_US
dc.subjectGenes, rasen_US
dc.subjectTOR Serine-Threonine Kinasesen_US
dc.titleInsights into significance of combined inhibition of MEK and m-TOR signalling output in KRAS mutant non-small-cell lung cancer.en_US
dc.typeJournal Article
dcterms.dateAccepted2016-06-23en_US
rioxxterms.funderThe Institute of Cancer Researchen_US
rioxxterms.identifier.projectUnspecifieden_US
rioxxterms.versionofrecord10.1038/bjc.2016.220en_US
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0en_US
rioxxterms.licenseref.startdate2016-08en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfBritish journal of canceren_US
pubs.issue5en_US
pubs.notesNo embargoen_US
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.publication-statusPublisheden_US
pubs.volume115en_US
pubs.embargo.termsNo embargoen_US
icr.researchteamClinical Pharmacology – Adaptive Therapyen_US
icr.researchteamMedicine Drug Development Unit (de Bono)en_US
dc.contributor.icrauthorBanerji, Udaien_US
dc.contributor.icrauthorTurner, Lydiaen_US
rioxxterms.funder.project354849bd-c553-4e22-868c-8c503e124155en_US


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