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@ARTICLE{Schupp:154767,
      author       = {J. Schupp and F. Krebs$^*$ and N. Zimmer and E. Trzeciak
                      and D. Schuppan and A. Tuettenberg},
      title        = {{T}argeting myeloid cells in the tumor sustaining
                      microenvironment.},
      journal      = {Cellular immunology},
      volume       = {343},
      issn         = {0008-8749},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2020-01014},
      pages        = {103713},
      year         = {2019},
      abstract     = {Myeloid cells are the most abundant cells in the tumor
                      microenvironment (TME). The tumor recruits and modulates
                      endogenous myeloid cells to tumor-associated macrophages
                      (TAM), dendritic cells (DC), myeloid-derived suppressor
                      cells (MDSC) and neutrophils (TAN), to sustain an
                      immunosuppressive environment. Pathologically overexpressed
                      mediators produced by cancer cells like
                      granulocyte-macrophage colony-stimulating- and vascular
                      endothelial growth factor induce myelopoiesis in the bone
                      marrow. Excess of myeloid cells in the blood, periphery and
                      tumor has been associated with tumor burden. In cancer,
                      myeloid cells are kept at an immature state of
                      differentiation to be diverted to an immunosuppressive
                      phenotype. Here, we review human myeloid cells in the TME
                      and the mechanisms for sustaining the hallmarks of cancer.
                      Simultaneously, we provide an introduction into current and
                      novel therapeutic approaches to redirect myeloid cells from
                      a cancer promoting to a rather inflammatory, cancer
                      inhibiting phenotype. In addition, the role of platelets for
                      tumor promotion is discussed.},
      subtyp        = {Review Article},
      cin          = {L501},
      ddc          = {610},
      cid          = {I:(DE-He78)L501-20160331},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29129292},
      doi          = {10.1016/j.cellimm.2017.10.013},
      url          = {https://inrepo02.dkfz.de/record/154767},
}