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@ARTICLE{Mogler:124436,
      author       = {C. Mogler$^*$ and C. König$^*$ and M. Wieland$^*$ and A.
                      Runge$^*$ and E. Besemfelder$^*$ and D. Komljenovic$^*$ and
                      T. Longerich and P. Schirmacher and H. G. Augustin},
      title        = {{H}epatic stellate cells limit hepatocellular carcinoma
                      progression through the orphan receptor endosialin.},
      journal      = {EMBO molecular medicine},
      volume       = {9},
      number       = {6},
      issn         = {1757-4684},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2017-01313},
      pages        = {741 - 749},
      year         = {2017},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Hepatocellular carcinoma (HCC) is among the most common and
                      deadliest cancers worldwide. A major contributor to HCC
                      progression is the cross talk between tumor cells and the
                      surrounding stroma including activated hepatic stellate
                      cells (HSC). Activation of HSC during liver damage leads to
                      upregulation of the orphan receptor endosialin (CD248),
                      which contributes to regulating the balance of liver
                      regeneration and fibrosis. Based on the established role of
                      endosialin in regulating HSC/hepatocyte cross talk, we
                      hypothesized that HSC-expressed endosialin might similarly
                      affect cell proliferation during hepatocarcinogenesis.
                      Indeed, the histological analysis of human HCC samples
                      revealed an inverse correlation between tumor cell
                      proliferation and stromal endosialin expression.
                      Correspondingly, global genetic inactivation of endosialin
                      resulted in accelerated tumor growth in an inducible mouse
                      HCC model. A candidate-based screen of tumor lysates and
                      differential protein arrays of cultured HSC identified
                      several established hepatotropic cytokines, including IGF2,
                      RBP4, DKK1, and CCL5 as being negatively regulated by
                      endosialin. Taken together, the experiments identify
                      endosialin-expressing HSC as a negative regulator of HCC
                      progression.},
      cin          = {A190 / L101 / E020},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)L101-20160331 /
                      I:(DE-He78)E020-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28373218},
      pmc          = {pmc:PMC5452049},
      doi          = {10.15252/emmm.201607222},
      url          = {https://inrepo02.dkfz.de/record/124436},
}