Resistance to KRAS g12c inhibitors in non-small cell lung cancer

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dc.contributor.authorRecondo, Gonzalo
dc.contributor.authorCardona, Andrés Felipe
dc.contributor.authorBlaquier, Juan Bautista
dc.contributor.orcidCardona, Andrés Felipe [https://orcid.org/0000-0003-3525-4126]
dc.contributor.orcidBlaquier, Juan Bautista [https://orcid.org/0000-0002-7197-5986]
dc.date.accessioned2022-09-21T13:58:26Z
dc.date.available2022-09-21T13:58:26Z
dc.date.issued2021
dc.description.abstractenglishKRAS mutations are one of the most prevalent oncogenic alterations in cancer. Until recently, drug development targeting KRAS did not convey clinical benefits to patients. Specific KRASG12C inhibitors, such as sotorasib and adagrasib, have been designed to bind to the protein’s mutant structure and block KRASG12C in its GDP-bound inactive state. Phase 1/2 trials have shown promising anti-tumor activity, especially in pretreated non-small cell lung cancer patients. As expected, both primary and secondary resistance to KRASG12C inhibitors invariably occurs, and molecular mechanisms have been characterized in pre-clinical models and patients. Several mechanisms such as tyrosine kinase receptors (RTKs) mediated feedback reactivation of ERK-dependent signaling can result in intrinsic resistance to KRAS target therapy. Acquired resistance to KRASG12C inhibitors include novel KRAS mutations such as Y96D/C and other RAS-MAPK effector protein mutations. This review focuses on the intrinsic and acquired mechanisms of resistance to KRASG12C inhibitors in KRASG12C mutant non-small cell lung cancer and the potential clinical strategies to overcome or prevent it.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.3389/fonc.2021.787585
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn2234-943X
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlrepourl:https://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/9069
dc.language.isoeng
dc.publisherFrontiers Media S.A.spa
dc.publisher.journalFrontiers in Oncologyspa
dc.relation.ispartofseriesFrontiers in Oncology, 2234-943X, Vol 11, 2021spa
dc.relation.urihttps://www.frontiersin.org/articles/10.3389/fonc.2021.787585/full
dc.rightsAtribución 4.0 Internacional*
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abierto
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.keywordsKRASG12Cspa
dc.subject.keywordsNSCLCspa
dc.subject.keywordsResistance mechanismsspa
dc.subject.keywordsTarget therapyspa
dc.subject.keywordsY96Dspa
dc.titleResistance to KRAS g12c inhibitors in non-small cell lung cancerspa
dc.title.translatedResistance to KRAS g12c inhibitors in non-small cell lung cancerspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.coarversionhttps://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

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