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@ARTICLE{OConnor:144843,
      author       = {T. O'Connor$^*$ and X. Zhou and J. Kosla$^*$ and A. Adili
                      and M. Garcia Beccaria$^*$ and E. Kotsiliti$^*$ and D.
                      Pfister$^*$ and A.-L. Johlke and A. Sinha and R. Sankowski
                      and M. Schick and R. Lewis and N. Dokalis and B. Seubert and
                      B. Höchst and D. Inverso$^*$ and D. Heide$^*$ and W. Zhang
                      and P. Weihrich and K. Manske and D. Wohlleber and M. Anton
                      and A. Hoellein and G. Seleznik and J. Bremer and S. Bleul
                      and H. G. Augustin$^*$ and F. Scherer and U. Koedel and A.
                      Weber and U. Protzer and R. Förster and T. Wirth and A.
                      Aguzzi and F. Meissner and M. Prinz and B. Baumann and U. E.
                      Höpken and P. A. Knolle and L. von Baumgarten and U. Keller
                      and M. Heikenwälder$^*$},
      title        = {{A}ge-{R}elated {G}liosis {P}romotes {C}entral {N}ervous
                      {S}ystem {L}ymphoma through {CCL}19-{M}ediated {T}umor
                      {C}ell {R}etention.},
      journal      = {Cancer cell},
      volume       = {36},
      number       = {3},
      issn         = {1535-6108},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-02268},
      pages        = {250 - 267.e9},
      year         = {2019},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {How lymphoma cells (LCs) invade the brain during the
                      development of central nervous system lymphoma (CNSL) is
                      unclear. We found that NF-κB-induced gliosis promotes CNSL
                      in immunocompetent mice. Gliosis elevated cell-adhesion
                      molecules, which increased LCs in the brain but was
                      insufficient to induce CNSL. Astrocyte-derived CCL19 was
                      required for gliosis-induced CNSL. Deleting CCL19 in mice or
                      CCR7 from LCs abrogated CNSL development. Two-photon
                      microscopy revealed LCs transiently entering normal brain
                      parenchyma. Astrocytic CCL19 enhanced parenchymal CNS
                      retention of LCs, thereby promoting CNSL formation. Aged,
                      gliotic wild-type mice were more susceptible to forming CNSL
                      than young wild-type mice, and astrocytic CCL19 was observed
                      in both human gliosis and CNSL. Therefore, CCL19-CCR7
                      interactions may underlie an increased age-related risk for
                      CNSL.},
      cin          = {F180 / A190 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)A190-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {316 - Infections and cancer (POF3-316)},
      pid          = {G:(DE-HGF)POF3-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31526758},
      doi          = {10.1016/j.ccell.2019.08.001},
      url          = {https://inrepo02.dkfz.de/record/144843},
}