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@ARTICLE{Kruchen:274483,
      author       = {A. Kruchen and P. Johann$^*$ and L. Rekowski and I.
                      Müller},
      title        = {{E}pigenetic {M}odification of {M}esenchymal {S}tromal
                      {C}ells {D}erived from {B}one {M}arrow and {E}mbryonal
                      {T}umors to {F}acilitate {I}mmunotherapeutic {A}pproaches in
                      {P}ediatric {M}alignancies.},
      journal      = {Current issues in molecular biology},
      volume       = {45},
      number       = {3},
      issn         = {1467-3037},
      address      = {Wymondham, Norfolk},
      reportid     = {DKFZ-2023-00626},
      pages        = {2121 - 2135},
      year         = {2023},
      abstract     = {Mesenchymal stromal cells (MSC) are part of the bone marrow
                      architecture and contribute to the homeostasis of
                      hematopoietic stem cells. Moreover, they are known to
                      regulate immune effector cells. These properties of MSC are
                      pivotal under physiologic conditions, and they may
                      aberrantly also protect malignant cells. MSCs are also found
                      in the leukemic stem cell niche of the bone marrow and as
                      part of the tumor microenvironment. Here, they protect
                      malignant cells from chemotherapeutic drugs and from immune
                      effector cells in immunotherapeutic approaches. Modulation
                      of these mechanisms may improve the efficacy of therapeutic
                      regimens. We investigated the effect of the histone
                      deacetylase inhibitor (HDACi) suberoylanilide hydroxamic
                      acid (SAHA, Vorinostat™) on the immunomodulatory effect
                      and cytokine profile of MSC derived from bone marrow and
                      pediatric tumors. The immune phenotype of MSC was not
                      markedly affected. SAHA-treated MSC showed reduced
                      immunomodulatory effects on T cell proliferation and NK cell
                      cytotoxicity. This effect was accompanied by an altered
                      cytokine profile of MSC. While untreated MSC inhibited the
                      production of certain pro-inflammatory cytokines, SAHA
                      treatment led to a partial increase in IFNγ and TNFα
                      secretion. These alterations of the immunosuppressive milieu
                      might be beneficial for immunotherapeutic approaches.},
      keywords     = {histone deacetylase inhibitor (Other) / leukemic stem cell
                      niche (Other) / mesenchymal stromal cells (Other) / tumor
                      microenvironment (Other)},
      cin          = {B062 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36975506},
      doi          = {10.3390/cimb45030136},
      url          = {https://inrepo02.dkfz.de/record/274483},
}