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dc.contributor.authorLopez, Sophie
dc.contributor.authorVoisset, Edwige
dc.contributor.authorTisserand, Julie C
dc.contributor.authorMosca, Cyndie
dc.contributor.authorPrebet, Thomas
dc.contributor.authorSantamaria D, David 
dc.contributor.authorDubreuil, Patrice
dc.contributor.authorDe Sepulveda, Paulo
dc.date.accessioned2019-12-23T14:10:46Z
dc.date.available2019-12-23T14:10:46Z
dc.date.issued2016-08-09
dc.identifier.citationOncotarget. 2016;7 (32):51163-51173.es_ES
dc.identifier.issn1949-2553es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8876
dc.description.abstractCDK4/CDK6 and RB proteins drive the progression through the G1 phase of the cell cycle. In acute myeloid leukemia (AML), the activity of the CDK/Cyclin D complex is increased. The mechanism involved is unknown, as are the respective roles played by CDK4 or CDK6 in this process. Here, we report that AML cells carrying FLT3-ITD mutations are dependent on CDK6 for cell proliferation while CDK4 is not essential. We showed that FLT3-ITD signaling is responsible for CDK6 overexpression, through a pathway involving the SRC-family kinase HCK. Accordingly, FLT3-ITD failed to transform primary hematopoietic progenitor cells from Cdk6-/- mice. Our results demonstrate that CDK6 is the primary target of CDK4/CDK6 inhibitors in FLT3-ITD positive AML. Furthermore, we delineate an essential protein kinase pathway -FLT3/HCK/CDK6- in the context of AML with FLT3-ITD mutations.es_ES
dc.description.sponsorshipThis project was supported by La Ligue Contre le Cancer (Equipe labelisee) and a grant from the Fondation ARC pour la Recherche sur le Cancer.es_ES
dc.language.isoenges_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectAMLes_ES
dc.subjectSRCes_ES
dc.subjectoncogenees_ES
dc.subjectpalbociclibes_ES
dc.subjectprotein kinasees_ES
dc.subjectsignalinges_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCell Line, Tumor es_ES
dc.subject.meshCyclin-Dependent Kinase 6 es_ES
dc.subject.meshGene Expression Regulation, Leukemic es_ES
dc.subject.meshHumans es_ES
dc.subject.meshLeukemia, Myeloid, Acute es_ES
dc.subject.meshMice es_ES
dc.subject.meshMice, Inbred C57BL es_ES
dc.subject.meshMice, Knockout es_ES
dc.subject.meshMutation es_ES
dc.subject.meshProto-Oncogene Proteins c-hck es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshTandem Repeat Sequences es_ES
dc.subject.meshfms-Like Tyrosine Kinase 3 es_ES
dc.titleAn essential pathway links FLT3-ITD, HCK and CDK6 in acute myeloid leukemiaes_ES
dc.typeArtículoes_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID27323399es_ES
dc.format.volume7es_ES
dc.format.number32es_ES
dc.format.page51163-51173es_ES
dc.identifier.doi10.18632/oncotarget.9965es_ES
dc.contributor.funderLa Ligue Contre le Cancer (Equipe labelisee)es_ES
dc.contributor.funderFondation ARC pour la Recherche sur le Canceres_ES
dc.identifier.e-issn1949-2553es_ES
dc.relation.publisherversionhttps://doi.org/10.18632/oncotarget.9965es_ES
dc.identifier.journalOncotargetes_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Oncología Experimentales_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Atribución-NoComercial-CompartirIgual 4.0 Internacional
This item is licensed under a: Atribución-NoComercial-CompartirIgual 4.0 Internacional