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dc.contributor.authorHervieu, Aen_US
dc.contributor.authorKermorgant, Sen_US
dc.coverage.spatialSwitzerlanden_US
dc.date.accessioned2019-02-20T08:10:40Z
dc.date.issued2018en_US
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/30406111en_US
dc.identifier.citationFront Mol Biosci, 2018, 5 pp. 86 - ?en_US
dc.identifier.issn2296-889Xen_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/3068
dc.identifier.doi10.3389/fmolb.2018.00086en_US
dc.description.abstractThe Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signaling. Phosphatidylinositide 3-kinase (PI3K) is one of the most deregulated pathways in cancer and implicated in various types of cancer. PI3K signaling is also a major signaling pathway downstream of RTK, including Met. PI3K major effectors include Akt and "mechanistic Target of Rapamycin" (mTOR), which each play key roles in numerous and various cell functions. Advancements made due to the development of molecular and pharmaceutical tools now allow us to delve into the roles of each independently. In this review, we summarize the current understanding we possess of the activation and role of PI3K/Akt/mTOR, downstream of Met, in cancer.en_US
dc.format.extent86 - ?en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.subjectAkten_US
dc.subjectMeten_US
dc.subjectPI3Ken_US
dc.subjectcanceren_US
dc.subjectmTORen_US
dc.subjectsignalingen_US
dc.titleThe Role of PI3K in Met Driven Cancer: A Recap.en_US
dc.typeJournal Article
dcterms.dateAccepted2018-09-10en_US
rioxxterms.versionofrecord10.3389/fmolb.2018.00086en_US
rioxxterms.licenseref.startdate2018en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfFront Mol Bioscien_US
pubs.notesNot knownen_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/Signal Transduction & Molecular Pharmacology
pubs.publication-statusPublished onlineen_US
pubs.volume5en_US
pubs.embargo.termsNot knownen_US
icr.researchteamSignal Transduction & Molecular Pharmacologyen_US
dc.contributor.icrauthorHervieu Vilches, Alexiaen_US


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