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@ARTICLE{Kennel:274326,
      author       = {K. B. Kennel and M. Bozlar and A. F. De Valk and F. R.
                      Greten$^*$},
      title        = {{C}ancer-{A}ssociated {F}ibroblasts in {I}nflammation and
                      {A}ntitumor {I}mmunity.},
      journal      = {Clinical cancer research},
      volume       = {29},
      number       = {6},
      issn         = {1078-0432},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DKFZ-2023-00540},
      pages        = {1009 - 1016},
      year         = {2023},
      abstract     = {Tumor-associated inflammation (TAI) is a feature of
                      essentially all cancers and can confer both tumor-promoting
                      and -suppressive functions. Cancer-associated fibroblasts
                      (CAF) comprise one very heterogeneous cellular component of
                      the tumor microenvironment characterized by a high degree of
                      plasticity. Recent single-cell sequencing analyses revealed
                      distinct CAF populations in various human cancers and helped
                      to define key CAF subtypes, such as myofibroblastic,
                      inflammatory, and antigen-presenting CAFs, with the first
                      two being present in virtually all tumors. Importantly,
                      these three CAF populations are involved in and modulate the
                      positive and negative consequences of TAI. The remarkable
                      plasticity of CAFs allows them to shift phenotypically and
                      functionally in response to environmental changes. In this
                      review, we describe how CAFs nurture tumor-promoting
                      inflammation and suppress adaptive immunity. We also
                      summarize the recently emerging evidence pertaining to
                      tumor-suppressive CAF functions in the context of TAI.
                      Finally, we summarize therapeutic concepts that aim at
                      modulating CAF functions or depleting immunosuppressive CAFs
                      to synergize with immunotherapy.},
      subtyp        = {Review Article},
      keywords     = {Humans / Cancer-Associated Fibroblasts: pathology /
                      Neoplasms: genetics / Neoplasms: pathology / Inflammation:
                      pathology / Tumor Microenvironment / Fibroblasts},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36399325},
      pmc          = {pmc:PMC10011884},
      doi          = {10.1158/1078-0432.CCR-22-1031},
      url          = {https://inrepo02.dkfz.de/record/274326},
}