A Braf kinase-inactive mutant induces lung adenocarcinoma

Patricia Nieto, Chiara Ambrogio, Laura Esteban-Burgos, Gonzalo Gómez-López, María Teresa Blasco, Zhan Yao, Richard Marais, Neal Rosen, Roberto Chiarle, David G. Pisano, Mariano Barbacid () and David Santamaría ()
Additional contact information
Patricia Nieto: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
Chiara Ambrogio: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
Laura Esteban-Burgos: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
Gonzalo Gómez-López: Bioinformatics Unit, Structural Biology and Biocomputing Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
María Teresa Blasco: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
Zhan Yao: Program in Molecular Pharmacology, Memorial Sloan-Kettering Cancer Center
Richard Marais: Molecular Oncology Group, Cancer Research UK Manchester Institute
Neal Rosen: Program in Molecular Pharmacology, Memorial Sloan-Kettering Cancer Center
Roberto Chiarle: Harvard Medical School, Boston Children’s Hospital
David G. Pisano: Bioinformatics Unit, Structural Biology and Biocomputing Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
Mariano Barbacid: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)
David Santamaría: Experimental Oncology, Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO)

Nature, 2017, vol. 548, issue 7666, 239-243

Abstract: Kinase-inactive Braf mutants can initiate the development of lung adenocarcinoma in mice; co-expression of activated Kras enhances tumour initiation and progression, and wild-type Braf is required to sustain tumorigenesis.

Date: 2017
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DOI: 10.1038/nature23297

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