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@ARTICLE{Baumann:169933,
      author       = {D. Baumann$^*$ and J. Drebant$^*$ and T. Hägele$^*$ and L.
                      Burger$^*$ and C. Serger$^*$ and C. Lauenstein$^*$ and P.
                      Dudys and G. Erdmann and R. Offringa$^*$},
      title        = {p38 {MAPK} signaling in {M}1 macrophages results in
                      selective elimination of {M}2 macrophages by {MEK}
                      inhibition.},
      journal      = {Journal for ImmunoTherapy of Cancer},
      volume       = {9},
      number       = {7},
      issn         = {2051-1426},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2021-01639},
      pages        = {e002319},
      year         = {2021},
      note         = {#EA:D200#LA:D200#},
      abstract     = {M2 macrophages promote tumor progression and therapy
                      resistance, whereas proimmunogenic M1 macrophages can
                      contribute to the efficacy of cytostatic and
                      immunotherapeutic strategies. The abundance of M2
                      macrophages in the immune infiltrate of many cancer types
                      has prompted the search for strategies to target and
                      eliminate this subset. From our prior experiments in
                      syngeneic mouse tumor models, we learned that
                      pharmacological inhibition of mitogen-activated protein
                      kinase kinase (MEK) did not merely result in tumor cell
                      death, but also in the modulation of the tumor immune
                      infiltrate. This included a prominent decrease in the
                      numbers of macrophages as well as an increase in the M1/M2
                      macrophage ratio. Investigation of the mechanism underlying
                      this finding in primary murine macrophage cultures revealed
                      that M2 macrophages are significantly more sensitive to MEK
                      inhibition-induced cell death than their M1 counterparts.
                      Further analyses showed that the p38 MAPK pathway, which is
                      activated in M1 macrophages only, renders these cells
                      resistant to death by MEK inhibition. In conclusion, the
                      dependency of M2 macrophages on the MEK/extracellular-signal
                      regulated kinase (ERK) pathway empowers MEK inhibitors to
                      selectively eliminate this subset from the tumor
                      microenvironment.},
      keywords     = {drug evaluation (Other) / immunomodulation (Other) /
                      macrophages (Other) / preclinical (Other) / tumor
                      microenvironment (Other)},
      cin          = {D200},
      ddc          = {610},
      cid          = {I:(DE-He78)D200-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34285105},
      doi          = {10.1136/jitc-2020-002319},
      url          = {https://inrepo02.dkfz.de/record/169933},
}