The ERBB network facilitates KRAS-driven lung tumorigenesis
Björn Kruspig(University of Glasgow), Tiziana Monteverde(University of Glasgow), Sarah Neidler(University of Glasgow), Andreas Hock(Cancer Research UK Scotland Institute), Emma Kerr(MRC Cancer Unit), Colin Nixon(Cancer Research UK Scotland Institute), William Clark(Cancer Research UK Scotland Institute), Ann Hedley(Cancer Research UK Scotland Institute), Sarah Laing(University of Glasgow), Seth B. Coffelt(University of Glasgow), John Le Quesne(MRC Toxicology Unit), Craig Dick(Queen Elizabeth University Hospital), Karen H. Vousden(Cancer Research UK Scotland Institute), Carla P. Martins(MRC Cancer Unit), Daniel J. Murphy(Cancer Research UK Scotland Institute)
Cited by 111Open Access
Abstract
-driven lung tumors. We present evidence that ERBB activity amplifies signaling through the core RAS pathway, supporting proliferation of KRAS-mutant tumor cells in culture and progression to invasive disease in vivo. Brief pharmacological inhibition of the ERBB network enhances the therapeutic benefit of MEK (mitogen-activated protein kinase kinase) inhibition in an autochthonous tumor setting. Our data suggest that lung cancer patients with KRAS-driven disease may benefit from inclusion of multi-ERBB inhibitors in rationally designed treatment strategies.
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