TY  - GEN
AU  - de-la-Puente-Ovejero, Laura
AU  - Fernández-Rodríguez, Ana
AU  - Francoz, Sarah
AU  - Aizpurua, Gonzalo
AU  - Lomba-Riego, Lucía
AU  - Drosten, Matthias
AU  - Guerra, Carmen
AU  - Musteanu, Mónica
AU  - Barbacid, Mariano
AU  - García-Alonso, Sara
PY  - 2026
UR  - https://hdl.handle.net/20.500.12105/27498
AB  - 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...
AB  - We used dual-recombinase genetically engineered mouse models of Kras+/G12V;Trp53-/- lung cancer to evaluate the effects of Raf1 ablation alone or in combination with Araf, Egfr, or Ddr1. Lung tumors were initiated by intranasal Ad5-CMV-FLPo delivery...
AB  - Raf1 deletion induced robust tumor regression within two months, in more than 60% of lesions. Araf ablation alone or combined with Raf1 did not affect tumor initiation, progression, or regression rates. Similarly, neither genetic nor pharmacological...
AB  - RAF1 is a key, non-redundant vulnerability in KRAS-driven lung adenocarcinoma. Co-targeting ARAF, EGFR, or DDR1 provides no additional therapeutic benefit in established disease. The absence of adverse effects from ARAF co-deletion suggests that RAF1...
LA  - eng
PB  - PUBLIC LIBRARY SCIENCE
KW  - K-RAS ONCOGENE
KW  - A-RAF
KW  - B-RAF
KW  - PROTEIN-KINASE
KW  - APOPTOSIS
KW  - MICE
KW  - REGRESSION
KW  - MUTATIONS
KW  - LETHALITY
TI  - RAF1 as a standalone therapeutic target in KRAS-driven lung adenocarcinoma: No added efficacy from co-targeting ARAF, EGFR, or DDR1.
TY  - research article
ER  -