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@ARTICLE{Hongu:179697,
      author       = {T. Hongu$^*$ and M. Pein$^*$ and J. Insua-Rodríguez$^*$
                      and E. Gutjahr and G. Mattavelli and J. Meier$^*$ and K.
                      Decker$^*$ and A. Descot$^*$ and M. Bozza$^*$ and R.
                      Harbottle$^*$ and A. Trumpp$^*$ and H.-P. Sinn and A.
                      Riedel$^*$ and T. Oskarsson$^*$},
      title        = {{P}erivascular tenascin {C} triggers sequential activation
                      of macrophages and endothelial cells to generate a
                      pro-metastatic vascular niche in the lungs.},
      journal      = {Nature cancer},
      volume       = {3},
      number       = {4},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2022-00846},
      pages        = {486-504},
      year         = {2022},
      note         = {#EA:A010#LA:A010# / 2022 Apr;3(4):486-504},
      abstract     = {Disseminated cancer cells frequently lodge near vasculature
                      in secondary organs. However, our understanding of the
                      cellular crosstalk invoked at perivascular sites is still
                      rudimentary. Here, we identify intercellular machinery
                      governing formation of a pro-metastatic vascular niche
                      during breast cancer colonization in the lung. We show that
                      specific secreted factors, induced in metastasis-associated
                      endothelial cells (ECs), promote metastasis in mice by
                      enhancing stem cell properties and the viability of cancer
                      cells. Perivascular macrophages, activated via tenascin C
                      (TNC) stimulation of Toll-like receptor 4 (TLR4), were shown
                      to be crucial in niche activation by secreting nitric oxide
                      (NO) and tumor necrosis factor (TNF) to induce EC-mediated
                      production of niche components. Notably, this mechanism was
                      independent of vascular endothelial growth factor (VEGF), a
                      key regulator of EC behavior and angiogenesis. However,
                      targeting both macrophage-mediated vascular niche activation
                      and VEGF-regulated angiogenesis resulted in added potency to
                      curb lung metastasis in mice. Together, our findings provide
                      mechanistic insights into the formation of vascular niches
                      in metastasis.},
      cin          = {A010 / F160 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)A010-20160331 / I:(DE-He78)F160-20160331 /
                      I:(DE-He78)HD01-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35469015},
      doi          = {10.1038/s43018-022-00353-6},
      url          = {https://inrepo02.dkfz.de/record/179697},
}