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@ARTICLE{Ivanova:181400,
      author       = {E. Ivanova$^*$ and B. Costa$^*$ and T. Eisemann$^*$ and S.
                      Lohr$^*$ and P. Boskovic$^*$ and V. Eichwald$^*$ and J.
                      Meckler$^*$ and M. Jugold$^*$ and V. Orian-Rousseau and H.
                      Peterziel$^*$ and P. Angel$^*$},
      title        = {{CD}44 expressed by myeloid cells promotes glioma
                      invasion.},
      journal      = {Frontiers in oncology},
      volume       = {12},
      issn         = {2234-943X},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2022-01968},
      pages        = {969787},
      year         = {2022},
      note         = {DKFZ/ZMBH Alliance /#EA: A100#LA:A100#},
      abstract     = {Glioblastoma multiforme (GBM) is one of the most common and
                      malignant brain tumors in adulthood with a median survival
                      of only 15 months. This poor prognosis is related to GBM's
                      ability to extensively infiltrate the surrounding brain
                      parenchyma resulting in diffuse spread of neoplastic cells
                      in the brain, responsible for high rate of recurrence. CD44
                      (Cluster of Differentiation 44) is a transmembrane protein,
                      overexpressed in multiple cancer types, including gliomas,
                      and implicated in cell motility, proliferation and
                      angiogenesis. Multiple studies have investigated the role of
                      CD44 in GBM cells and have highlighted a link between tumor
                      malignancy and CD44 expression. However up to date, little
                      is known of the role of CD44 on cells from the tumor
                      microenvironment (TME). Here, we have investigated a
                      potential role of CD44 in the TME in regards to GBM
                      invasiveness. Using an ex-vivo organotypic brain slice
                      invasion assay, we show that absence of CD44 from the TME
                      impairs the ability of glioma cells to invade the
                      surrounding brain parenchyma. By deleting CD44 in the
                      astrocytic, endothelial and myeloid compartments, we show
                      that it is specifically CD44 expression in myeloid cells
                      that is responsible for the observed phenotype. Combining in
                      vivo studies in cell-specific knock-out mice and in vitro
                      analyses on primary microglia we demonstrate that myeloid
                      CD44 is implicated in Toll Like Receptor 2 signaling and is
                      a major regulator of Matrix metalloproteinase 9 expression.},
      keywords     = {CD44 (Other) / MMP9 (Other) / TLR2 (Other) / glioblastoma
                      (Other) / microglia (Other) / tumor microenvironment
                      (Other)},
      cin          = {A100 / W240 / B310},
      ddc          = {610},
      cid          = {I:(DE-He78)A100-20160331 / I:(DE-He78)W240-20160331 /
                      I:(DE-He78)B310-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35992852},
      pmc          = {pmc:PMC9386454},
      doi          = {10.3389/fonc.2022.969787},
      url          = {https://inrepo02.dkfz.de/record/181400},
}