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      Evaluating the landscape of gene cooperativity with receptor tyrosine kinases in liver tumorigenesis using transposon-mediated mutagenesis.

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          Abstract

          The variety of alterations found in hepatocellular carcinoma (HCC) makes the identification of functionally relevant genes and their combinatorial actions in tumorigenesis challenging. Deregulation of receptor tyrosine kinases (RTKs) is frequent in HCC, yet little is known about the molecular events that cooperate with RTKs and whether these cooperative events play an active role at the root of liver tumorigenesis.

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          Author and article information

          Journal
          J. Hepatol.
          Journal of hepatology
          Elsevier BV
          1600-0641
          0168-8278
          March 2019
          : 70
          : 3
          Affiliations
          [1 ] Aix Marseille Univ, CNRS, Developmental Biology Institute of Marseille (IBDM) UMR 7288, Parc Scientifique de Luminy, Marseille, France.
          [2 ] Department of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
          [3 ] Computational Biology Group, Max Planck Institute of Biochemistry, Martinsried, Germany.
          [4 ] Aix Marseille Univ, CNRS, Developmental Biology Institute of Marseille (IBDM) UMR 7288, Parc Scientifique de Luminy, Marseille, France. Electronic address: flavio.maina@univ-amu.fr.
          Article
          S0168-8278(18)32578-9
          10.1016/j.jhep.2018.11.027
          30529386
          cccae435-bd3c-4f49-be9f-b2c88dcd164d
          History

          Oncogenes,Mouse model,Functional screening,Liver cancer,Hepatocellular carcinoma,Signalling,Receptor tyrosine kinases,HCC,Tumour suppressors

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