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@ARTICLE{OConnor:169932,
      author       = {T. L. O'Connor$^*$ and M. Heikenwälder$^*$},
      title        = {{CCL}2 in the {T}umor {M}icroenvironment.},
      journal      = {Advances in experimental medicine and biology},
      volume       = {1302},
      issn         = {0065-2598},
      address      = {[Heidelberg]},
      publisher    = {Springer},
      reportid     = {DKFZ-2021-01638},
      isbn         = {978-3-030-62657-0 (print)},
      pages        = {1-14},
      year         = {2021},
      note         = {#EA:F180#LA:F180#},
      abstract     = {The C-C motif chemokine ligand 2 (CCL2) is a crucial
                      mediator of immune cell recruitment during microbial
                      infections and tissue damage. CCL2 is also frequently
                      overexpressed in cancer cells and other cells in the tumor
                      microenvironment, and a large body of evidence indicates
                      that high CCL2 levels are associated with more aggressive
                      malignancies, a higher probability of metastasis, and poorer
                      outcomes in a wide range of cancers. CCL2 plays a role in
                      recruiting tumor-associated macrophages (TAMs), which adopt
                      a pro-tumorigenic phenotype and support cancer cell
                      survival, facilitate tumor cell invasion, and promote
                      angiogenesis. CCL2 also has direct, TAM-independent effects
                      on tumor cells and the tumor microenvironment, including
                      recruitment of other myeloid subsets and non-myeloid cells,
                      maintaining an immunosuppressive environment, stimulating
                      tumor cell growth and motility, and promoting angiogenesis.
                      CCL2 also plays important roles in the metastatic cascade,
                      such as creating a pre-metastatic niche in distant organs
                      and promoting tumor cell extravasation across endothelia.
                      Due to its many roles in tumorigenesis and metastatic
                      processes, the CCL2-CCR2 signaling axis is currently being
                      pursued as a potential therapeutic target for cancer.},
      keywords     = {Cell Line, Tumor / Chemokine CCL2: genetics / Chemokines /
                      Ligands / Receptors, CCR2: genetics / Tumor Microenvironment
                      / Angiogenesis (Other) / CCL2 (Other) / CCR2 (Other) /
                      Cancer (Other) / Extravasation (Other) / Immunity (Other) /
                      Immunosuppression (Other) / Invasion (Other) / MCP-1 (Other)
                      / Macrophage (Other) / Metastasis (Other) / Microenvironment
                      (Other) / NFκB (Other) / TAM (Other) / Tumor (Other) /
                      Chemokine CCL2 (NLM Chemicals) / Chemokines (NLM Chemicals)
                      / Ligands (NLM Chemicals) / Receptors, CCR2 (NLM Chemicals)},
      cin          = {F180},
      ddc          = {570},
      cid          = {I:(DE-He78)F180-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)3 / PUB:(DE-HGF)16},
      pubmed       = {pmid:34286437},
      doi          = {10.1007/978-3-030-62658-7_1},
      url          = {https://inrepo02.dkfz.de/record/169932},
}