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@ARTICLE{LaPorta:132492,
      author       = {S. La Porta$^*$ and L. Roth$^*$ and M. Singhal$^*$ and C.
                      Mogler$^*$ and C. Spegg$^*$ and B. Schieb$^*$ and X. Qu and
                      R. H. Adams and H. S. Baldwin and S. Savant and H.
                      Augustin$^*$},
      title        = {{E}ndothelial {T}ie1-mediated angiogenesis and vascular
                      abnormalization promote tumor progression and metastasis.},
      journal      = {The journal of clinical investigation},
      volume       = {128},
      number       = {2},
      issn         = {1558-8238},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2018-00179},
      pages        = {834 - 845},
      year         = {2018},
      note         = {DKFZ-ZMBH-Allianz},
      abstract     = {The endothelial tyrosine kinase receptor Tie1 remains
                      poorly characterized, largely owing to its orphan receptor
                      status. Global Tie1 inactivation causes late embryonic
                      lethality, thereby reflecting its importance during
                      development. Tie1 also plays pivotal roles during
                      pathologies such as atherosclerosis and tumorigenesis. In
                      order to study the contribution of Tie1 to tumor progression
                      and metastasis, we conditionally deleted Tie1 in endothelial
                      cells at different stages of tumor growth and metastatic
                      dissemination. Tie1 deletion during primary tumor growth in
                      mice led to a decrease in microvessel density and an
                      increase in mural cell coverage with improved vessel
                      perfusion. Reduced angiogenesis and enhanced vascular
                      normalization resulted in a progressive increase of
                      intratumoral necrosis that caused a growth delay only at
                      later stages of tumor progression. Concomitantly, surgical
                      removal of the primary tumor decreased the number of
                      circulating tumor cells, reduced metastasis, and prolonged
                      overall survival. Additionally, Tie1 deletion in
                      experimental murine metastasis models prevented
                      extravasation of tumor cells into the lungs and reduced
                      metastatic foci. Taken together, the data support Tie1 as a
                      therapeutic target by defining its regulatory functions
                      during angiogenesis and vascular abnormalization and
                      identifying its role during metastasis.},
      cin          = {A190 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29355844},
      pmc          = {pmc:PMC5785248},
      doi          = {10.1172/JCI94674},
      url          = {https://inrepo02.dkfz.de/record/132492},
}