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@ARTICLE{Arkhypov:163021,
      author       = {I. Arkhypov$^*$ and S. Lasser$^*$ and V. Petrova$^*$ and R.
                      Weber$^*$ and C. Groth$^*$ and J. Utikal$^*$ and P.
                      Altevogt$^*$ and V. Umansky$^*$},
      title        = {{M}yeloid {C}ell {M}odulation by {T}umor-{D}erived
                      {E}xtracellular {V}esicles.},
      journal      = {International journal of molecular sciences},
      volume       = {21},
      number       = {17},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2020-01812},
      pages        = {6319},
      year         = {2020},
      note         = {#EA:A370#LA:A370# / #DKFZ-MOST-Ca181#},
      abstract     = {Extracellular vesicles (EV) can carry proteins, RNA and
                      DNA, thus serving as communication tools between cells.
                      Tumor cells secrete EV, which can be taken up by surrounding
                      cells in the tumor microenvironment as well as by cells in
                      distant organs. Tumor-derived EV (TEV) contain factors
                      induced by tumor-associated hypoxia such as heat shock
                      proteins or a variety of microRNA (miRNA). The interaction
                      of TEV with tumor and host cells can promote cancer
                      angiogenesis, invasion and metastasis. Myeloid cells are
                      widely presented in tissues, comprise the majority of immune
                      cells and play an essential role in immune reactions and
                      tissue remodeling. However, in cancer, the differentiation
                      of myeloid cells and their functions are impaired, resulting
                      in tumor promotion. Such alterations are due to chronic
                      inflammatory conditions associated with cancer and are
                      mediated by the tumor secretome, including TEV. A high
                      capacity of myeloid cells to clear EV from circulation put
                      them in the central position in EV-mediated formation of
                      pre-metastatic niches. The exposure of myeloid cells to TEV
                      could trigger numerous signaling pathways. Progenitors of
                      myeloid cells alter their differentiation upon the contact
                      with TEV, resulting in the generation of myeloid-derived
                      suppressor cells (MDSC), inhibiting anti-tumor function of T
                      and natural killer (NK) cells and promoting thereby tumor
                      progression. Furthermore, TEV can augment MDSC
                      immunosuppressive capacity. Different subsets of mature
                      myeloid cells such as monocytes, macrophages, dendritic
                      cells (DC) and granulocytes take up TEV and acquire a
                      protumorigenic phenotype. However, the delivery of tumor
                      antigens to DC by TEV was shown to enhance their
                      immunostimulatory capacity. The present review will discuss
                      a diverse and complex EV-mediated crosstalk between tumor
                      and myeloid cells in the context of the tumor type,
                      TEV-associated cargo molecules and type of recipient cells.},
      subtyp        = {Review Article},
      cin          = {A370},
      ddc          = {540},
      cid          = {I:(DE-He78)A370-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32878277},
      doi          = {10.3390/ijms21176319},
      url          = {https://inrepo02.dkfz.de/record/163021},
}