RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1.
KRAS-mutant lung adenocarcinoma remains without effective targeted therapies for most patients, particularly those with non-G12C alleles or resistance to KRASG12C inhibitors. RAF1 is essential for KRAS-driven tumor maintenance through kinase-independent survival functions, making it an attractive ca...
| Autores: | , , , , , , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Fecha de publicación: | 2026 |
| País: | España |
| Institución: | Instituto de Salud Carlos III (ISCIII) |
| Repositorio: | Repisalud |
| Idioma: | inglés |
| OAI Identifier: | oai:dnet:repisalud__::a3776a84b1e4f18ec66c8018666f660f |
| Acceso en línea: | https://hdl.handle.net/20.500.12105/27498 |
| Access Level: | acceso abierto |
| Palabra clave: | K-RAS ONCOGENE A-RAF B-RAF PROTEIN-KINASE APOPTOSIS MICE REGRESSION MUTATIONS LETHALITY |
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RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1.de-la-Puente-Ovejero, LauraFernández-Rodríguez, AnaFrancoz, SarahAizpurua, GonzaloLomba-Riego, LucíaDrosten, MatthiasGuerra, CarmenMusteanu, MónicaBarbacid, MarianoGarcía-Alonso, SaraK-RAS ONCOGENEA-RAFB-RAFPROTEIN-KINASEAPOPTOSISMICEREGRESSIONMUTATIONSLETHALITYKRAS-mutant lung adenocarcinoma remains without effective targeted therapies for most patients, particularly those with non-G12C alleles or resistance to KRASG12C inhibitors. RAF1 is essential for KRAS-driven tumor maintenance through kinase-independent survival functions, making it an attractive candidate for targeted protein degradation. However, the therapeutic impact and safety of co-targeting RAF1 with related kinases remain unclear.PUBLIC LIBRARY SCIENCEmadridComunidad de Madrid (España)Ministerio de Ciencia e Innovación (España)Fundación La CaixaCentro de Investigación Biomédica en Red - CIBERONC (Cáncer)Agencia Estatal de Investigación (España)20262026-06-0220262026-01-0120262026-01-01research articlehttp://purl.org/coar/resource_type/c_2df8fbb1VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttps://hdl.handle.net/20.500.12105/27498reponame:Repisaludinstname:Instituto de Salud Carlos III (ISCIII)InglésengAgencia Estatal de Investigación http://dx.doi.org/10.13039/501100011033 Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020 RTI2018-094664-B-I00 C-RAF, UN MEDIADOR CLAVE EN TUMORES INDUCIDOS POR EL ONCOGEN K-RAS: ESTRATEGIAS TERAPEUTICASopen accesshttp://purl.org/coar/access_right/c_abf2Attribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessoai:dnet:repisalud__::a3776a84b1e4f18ec66c8018666f660f2026-06-12T12:43:37Z |
| dc.title.none.fl_str_mv |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| title |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| spellingShingle |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. de-la-Puente-Ovejero, Laura K-RAS ONCOGENE A-RAF B-RAF PROTEIN-KINASE APOPTOSIS MICE REGRESSION MUTATIONS LETHALITY |
| title_short |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| title_full |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| title_fullStr |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| title_full_unstemmed |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| title_sort |
RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1. |
| dc.creator.none.fl_str_mv |
de-la-Puente-Ovejero, Laura Fernández-Rodríguez, Ana Francoz, Sarah Aizpurua, Gonzalo Lomba-Riego, Lucía Drosten, Matthias Guerra, Carmen Musteanu, Mónica Barbacid, Mariano García-Alonso, Sara |
| author |
de-la-Puente-Ovejero, Laura |
| author_facet |
de-la-Puente-Ovejero, Laura Fernández-Rodríguez, Ana Francoz, Sarah Aizpurua, Gonzalo Lomba-Riego, Lucía Drosten, Matthias Guerra, Carmen Musteanu, Mónica Barbacid, Mariano García-Alonso, Sara |
| author_role |
author |
| author2 |
Fernández-Rodríguez, Ana Francoz, Sarah Aizpurua, Gonzalo Lomba-Riego, Lucía Drosten, Matthias Guerra, Carmen Musteanu, Mónica Barbacid, Mariano García-Alonso, Sara |
| author2_role |
author author author author author author author author author |
| dc.contributor.none.fl_str_mv |
madrid Comunidad de Madrid (España) Ministerio de Ciencia e Innovación (España) Fundación La Caixa Centro de Investigación Biomédica en Red - CIBERONC (Cáncer) Agencia Estatal de Investigación (España) |
| dc.subject.none.fl_str_mv |
K-RAS ONCOGENE A-RAF B-RAF PROTEIN-KINASE APOPTOSIS MICE REGRESSION MUTATIONS LETHALITY |
| topic |
K-RAS ONCOGENE A-RAF B-RAF PROTEIN-KINASE APOPTOSIS MICE REGRESSION MUTATIONS LETHALITY |
| description |
KRAS-mutant lung adenocarcinoma remains without effective targeted therapies for most patients, particularly those with non-G12C alleles or resistance to KRASG12C inhibitors. RAF1 is essential for KRAS-driven tumor maintenance through kinase-independent survival functions, making it an attractive candidate for targeted protein degradation. However, the therapeutic impact and safety of co-targeting RAF1 with related kinases remain unclear. |
| publishDate |
2026 |
| dc.date.none.fl_str_mv |
2026 2026-06-02 2026 2026-01-01 2026 2026-01-01 |
| dc.type.none.fl_str_mv |
research article http://purl.org/coar/resource_type/c_2df8fbb1 VoR http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| dc.type.openaire.fl_str_mv |
info:eu-repo/semantics/article |
| format |
article |
| dc.identifier.none.fl_str_mv |
https://hdl.handle.net/20.500.12105/27498 |
| url |
https://hdl.handle.net/20.500.12105/27498 |
| dc.language.none.fl_str_mv |
Inglés eng |
| language_invalid_str_mv |
Inglés |
| language |
eng |
| dc.relation.none.fl_str_mv |
Agencia Estatal de Investigación http://dx.doi.org/10.13039/501100011033 Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020 RTI2018-094664-B-I00 C-RAF, UN MEDIADOR CLAVE EN TUMORES INDUCIDOS POR EL ONCOGEN K-RAS: ESTRATEGIAS TERAPEUTICAS |
| dc.rights.none.fl_str_mv |
open access http://purl.org/coar/access_right/c_abf2 Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ |
| dc.rights.openaire.fl_str_mv |
info:eu-repo/semantics/openAccess |
| rights_invalid_str_mv |
open access http://purl.org/coar/access_right/c_abf2 Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ |
| eu_rights_str_mv |
openAccess |
| dc.format.none.fl_str_mv |
application/pdf |
| dc.publisher.none.fl_str_mv |
PUBLIC LIBRARY SCIENCE |
| publisher.none.fl_str_mv |
PUBLIC LIBRARY SCIENCE |
| dc.source.none.fl_str_mv |
reponame:Repisalud instname:Instituto de Salud Carlos III (ISCIII) |
| instname_str |
Instituto de Salud Carlos III (ISCIII) |
| reponame_str |
Repisalud |
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Repisalud |
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