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@ARTICLE{Briest:282445,
      author       = {F. Briest and D. Noerenberg and C. Hennch and K. Yoshida
                      and R. Hablesreiter and J. Nimo and D. Sasca and M. Kirchner
                      and L. Mansouri and Y. Inoue and L. Wiegand and A. M.
                      Staiger and B. Casadei and P. Korkolopoulou and J. Weiner
                      and A. Lopez-Guillermo and A. Warth and T. Schneider and Á.
                      Nagy and W. Klapper and M. Hummel$^*$ and G. Kanellis and I.
                      Anagnostopoulos and P. Mertins and L. Bullinger$^*$ and R.
                      Rosenquist and T. P. Vassilakopoulos and G. Ott and S. Ogawa
                      and F. Damm$^*$},
      title        = {{F}requent {ZNF}217 mutations lead to transcriptional
                      deregulation of interferon signal transduction via altered
                      chromatin accessibility in {B} cell lymphoma.},
      journal      = {Leukemia},
      volume       = {37},
      number       = {11},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2023-01765},
      pages        = {2237-2249},
      year         = {2023},
      note         = {2023 Nov;37(11):2237-2249},
      abstract     = {Recent exome-wide studies discovered frequent somatic
                      mutations in the epigenetic modifier ZNF217 in primary
                      mediastinal B cell lymphoma (PMBCL) and related disorders.
                      As functional consequences of ZNF217 alterations remain
                      unknown, we comprehensively evaluated their impact in PMBCL.
                      Targeted sequencing identified genetic lesions affecting
                      ZNF217 in $33\%$ of 157 PMBCL patients. Subsequent gene
                      expression profiling (n = 120) revealed changes in cytokine
                      and interferon signal transduction in ZNF217-aberrant PMBCL
                      cases. In vitro, knockout of ZNF217 led to changes in
                      chromatin accessibility interfering with binding motifs for
                      crucial lymphoma-associated transcription factors. This led
                      to disturbed expression of interferon-responsive and
                      inflammation-associated genes, altered cell behavior, and
                      aberrant differentiation. Mass spectrometry demonstrates
                      that ZNF217 acts within a histone modifier complex
                      containing LSD1, CoREST and HDAC and interferes with H3K4
                      methylation and H3K27 acetylation. Concluding, our data
                      suggest non-catalytic activity of ZNF217, which directs
                      histone modifier complex function and controls B cell
                      differentiation-associated patterns of chromatin structure.},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37648814},
      doi          = {10.1038/s41375-023-02013-9},
      url          = {https://inrepo02.dkfz.de/record/282445},
}