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RANKL signaling sustains primary tumor growth in genetically engineered mouse models of lung adenocarcinoma
Julien Faget, Caroline Contat, Nadine Zangger, Solange Peters, View ORCID ProfileEtienne Meylan
doi: https://doi.org/10.1101/142620
Julien Faget
1Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.
Caroline Contat
1Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.
Nadine Zangger
1Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.
2Bioinformatics Core Facility, Swiss Institute of Bioinformatics, CH-1015 Lausanne, Switzerland.
Solange Peters
3Department of Oncology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, CH-1011 Lausanne, Switzerland.
Etienne Meylan
1Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.

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Posted May 26, 2017.
RANKL signaling sustains primary tumor growth in genetically engineered mouse models of lung adenocarcinoma
Julien Faget, Caroline Contat, Nadine Zangger, Solange Peters, Etienne Meylan
bioRxiv 142620; doi: https://doi.org/10.1101/142620
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