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@ARTICLE{Zhang:277705,
      author       = {L. Zhang$^*$ and M. Wirth$^*$ and U. Patra and J. Stroh$^*$
                      and K. Isaakidis$^*$ and L. Rieger and S. Kossatz$^*$ and M.
                      Milanovic$^*$ and C. Zang$^*$ and U. Demel$^*$ and J.
                      Keiten-Schmitz$^*$ and K. Wagner$^*$ and K. Steiger$^*$ and
                      R. Rad$^*$ and F. Bassermann$^*$ and S. Müller$^*$ and U.
                      Keller$^*$ and M. Schick$^*$},
      title        = {{A}ctionable loss of {SLF}2 drives {B}-cell lymphomagenesis
                      and impairs the {DNA} damage response.},
      journal      = {EMBO molecular medicine},
      volume       = {15},
      number       = {9},
      issn         = {1757-4676},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2023-01422},
      pages        = {e16431},
      year         = {2023},
      note         = {2023 Sep 11;15(9):e16431},
      abstract     = {The DNA damage response (DDR) acts as a barrier to
                      malignant transformation and is often impaired during
                      tumorigenesis. Exploiting the impaired DDR can be a
                      promising therapeutic strategy; however, the mechanisms of
                      inactivation and corresponding biomarkers are incompletely
                      understood. Starting from an unbiased screening approach, we
                      identified the SMC5-SMC6 Complex Localization Factor 2
                      (SLF2) as a regulator of the DDR and biomarker for a B-cell
                      lymphoma (BCL) patient subgroup with an adverse prognosis.
                      SLF2-deficiency leads to loss of DDR factors including
                      Claspin (CLSPN) and consequently impairs CHK1 activation. In
                      line with this mechanism, genetic deletion of Slf2 drives
                      lymphomagenesis in vivo. Tumor cells lacking SLF2 are
                      characterized by a high level of DNA damage, which leads to
                      alterations of the post-translational SUMOylation pathway as
                      a safeguard. The resulting co-dependency confers synthetic
                      lethality to a clinically applicable SUMOylation inhibitor
                      (SUMOi), and inhibitors of the DDR pathway act highly
                      synergistic with SUMOi. Together, our results identify SLF2
                      as a DDR regulator and reveal co-targeting of the DDR and
                      SUMOylation as a promising strategy for treating aggressive
                      lymphoma.},
      keywords     = {CHK1 (Other) / DNA damage response (Other) / SLF2 (Other) /
                      SUMO (Other) / lymphoma (Other)},
      cin          = {BE01 / FM01 / MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331 / I:(DE-He78)FM01-20160331 /
                      I:(DE-He78)MU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37485814},
      doi          = {10.15252/emmm.202216431},
      url          = {https://inrepo02.dkfz.de/record/277705},
}