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Targeting the MAPK Pathway in KRAS-Driven Tumors.

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dc.contributor.authorDrosten, Matthias
dc.contributor.authorBarbacid, Mariano
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC)
dc.contributor.funderUnión Europea. Comisión Europea
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)
dc.contributor.funderComunidad de Madrid (España)
dc.contributor.funderAsociación Española Contra el Cáncer
dc.contributor.funderFundación AXA
dc.date.accessioned2022-07-27T09:11:53Z
dc.date.available2022-07-27T09:11:53Z
dc.date.issued2020-04-13
dc.description.abstractKRAS mutations occur in a quarter of all of human cancers, yet no selective drug has been approved to treat these tumors. Despite the recent development of drugs that block KRASG12C, the majority of KRAS oncoproteins remain undruggable. Here, we review recent efforts to validate individual components of the mitogen-activated protein kinase (MAPK) pathway as targets to treat KRAS-mutant cancers by comparing genetic information derived from experimental mouse models of KRAS-driven lung and pancreatic tumors with the outcome of selective MAPK inhibitors in clinical trials. We also review the potential of RAF1 as a key target to block KRAS-mutant cancers.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipThis work was supported by grants from the European Research Council (ERC-AG/695566, THERACAN), the Spanish Ministry of Science, Innovation and Universities (RTI2018-094664-B-I00 and RTC2017-6576-1), the Autonomous Community of Madrid (B2017/BMD-3884 iLUNG-CM), and the Asociacion Espanola contra el Cancer (GC166173694BARB). M.B. is a recipient of an Endowed Chair from the AXA Research Fund.es_ES
dc.format.number4es_ES
dc.format.page543-550es_ES
dc.format.volume37es_ES
dc.identifier.citationCancer Cell . 2020;37(4):543-550.es_ES
dc.identifier.doi10.1016/j.ccell.2020.03.013es_ES
dc.identifier.e-issn1878-3686es_ES
dc.identifier.issn1535-6108es_ES
dc.identifier.journalCancer celles_ES
dc.identifier.pubmedID32289276es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/14770
dc.language.isoenges_ES
dc.publisherCell Press
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/RTI2018-094664-B-I00es_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/RTC2017-6576-1es_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/B2017/BMD-3884 iLUNG-CMes_ES
dc.relation.projectFISinfo:eu-repo/grantAgreement/ES/GC166173694BARBes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/EC/H2020/695566/EUes_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.ccell.2020.03.013.es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Oncología Experimentales_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshMolecular Targeted Therapyes_ES
dc.subject.meshMutationes_ES
dc.subject.meshHumanses_ES
dc.subject.meshMitogen-Activated Protein Kinaseses_ES
dc.subject.meshNeoplasmses_ES
dc.subject.meshProtein Kinase Inhibitorses_ES
dc.subject.meshProto-Oncogene Proteins p21(ras)es_ES
dc.titleTargeting the MAPK Pathway in KRAS-Driven Tumors.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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