Overcoming TKI resistance in fusion-driven NSCLC: New generation inhibitors and rationale for combination strategies

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dc.contributor.authorRusso, Alessandro
dc.contributor.authorCardona, Andrés F.
dc.contributor.authorCaglevic, Christian
dc.contributor.authorManca, Paolo
dc.contributor.authorRuiz Patiño, Alejandro
dc.contributor.authorArrieta, Oscar
dc.contributor.authorRolfo, Christian
dc.date.accessioned2021-05-21T21:54:28Z
dc.date.available2021-05-21T21:54:28Z
dc.date.issued2020-12
dc.description.abstractenglishDuring the last several years, multiple gene rearrangements with oncogenic potential have been described in NSCLC, identifying specific clinic-pathological subgroups of patients that benefit from a targeted therapeutic approach, including anaplastic lymphoma kinase (ALK), c-ros protooncogene 1 (ROS1) and,more recently, REarranged during Transfection (RET) and neurotrophic tyrosine receptor kinases (NTRK) genes. Despite initial impressive antitumor activity, the use of targeted therapies in oncogene-addicted NSCLC subgroups is invariably associated with the development of acquired resistance through multiple mechanisms that can include both on-target and off-target mechanisms. However, the process of acquired resistance is a rapidly evolving clinical scenario that constantly evolves under the selective pressure of tyrosine kinase inhibitors. The development of increasingly higher selective and potent inhibitors, traditionally used to overcome resistance to first generation inhibitors, is associated with the development of novel mechanisms of resistance that encompass complex resistance mutations, highly recalcitrant to available TKIs, and bypass track mechanisms. Herein, we provide a comprehensive overview on the therapeutic strategies for overcoming acquired resistance to tyrosine kinase inhibitors (TKIs) targeting the most well-established oncogenic gene fusions in advanced NSCLC, including ALK, ROS1, RET, and NTRK rearrangements.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.21037/TLCR-2019-CNSCLC-06
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn2226-4477
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlrepourl:https://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/5891
dc.language.isoeng
dc.publisherAME Publishing Companyspa
dc.publisher.journalTranslational Lung Cancer Researchspa
dc.relation.ispartofseriesTranslational Lung Cancer Research, 2226-4477, Vol. 9, Nro. 6, 2020, p. 2581-2598spa
dc.relation.urihttps://tlcr.amegroups.com/article/view/44424/html
dc.rightsAttribution-NonCommercial-NoDerivatives 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.localAcceso abiertospa
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.keywordsAnaplastic lymphoma kinase (ALK)spa
dc.subject.keywordsREarranged during Transfection (RET)spa
dc.subject.keywordsC-ros protooncogene 1 (ROS1)spa
dc.subject.keywordsNeurotrophic tyrosine receptor kinases (NTRK)spa
dc.subject.keywordsAcquired resistancespa
dc.titleOvercoming TKI resistance in fusion-driven NSCLC: New generation inhibitors and rationale for combination strategiesspa
dc.title.translatedOvercoming TKI resistance in fusion-driven NSCLC: New generation inhibitors and rationale for combination strategiesspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

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