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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.
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Caroline Contat
1Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland.
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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.
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Solange Peters
3Department of Oncology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, CH-1011 Lausanne, Switzerland.
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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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  • ORCID record for Etienne Meylan
  • For correspondence: etienne.meylan@epfl.ch
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Posted May 26, 2017.
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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, Etienne Meylan
bioRxiv 142620; doi: https://doi.org/10.1101/142620
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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, Etienne Meylan
bioRxiv 142620; doi: https://doi.org/10.1101/142620

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