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@ARTICLE{Riabinska:145055,
      author       = {Riabinska, Arina and Lehrmann, Daria and Jachimowicz, Ron
                      Daniel and Knittel, Gero and Fritz, Christian and Schmitt,
                      Anna and Geyer, Aenne and Heneweer, Carola and Wittersheim,
                      Maike and Frenzel, Lukas P and Torgovnick, Alessandro and
                      Wiederstein, Janica Lea and Wunderlich, Claudia Maria and
                      Ortmann, Monika and Paillard, Arlette and Wößmann, Wilhelm
                      and Borkhardt, Arndt and Burdach, Stefan and Hansmann,
                      Martin-Leo and Rosenwald, Andreas and Perner, Sven and Mall,
                      Gita and Klapper, Wolfram and Merseburg, Andrea and Krüger,
                      Marcus and Grüll, Holger and Persigehl, Thorsten and
                      Wunderlich, Frank Thomas and Peifer, Martin and Utermöhlen,
                      Olaf and Büttner, Reinhard and Beleggia, Filippo and
                      Reinhardt, Hans Christian},
      title        = {{ATM} activity in {T} cells is critical for immune
                      surveillance of lymphoma in vivo.},
      journal      = {Leukemia},
      volume       = {34},
      number       = {3},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2020-00415},
      pages        = {771-786},
      year         = {2020},
      abstract     = {The proximal DNA damage response kinase ATM is frequently
                      inactivated in human malignancies. Germline mutations in the
                      ATM gene cause Ataxia-telangiectasia (A-T), characterized by
                      cerebellar ataxia and cancer predisposition. Whether ATM
                      deficiency impacts on tumor initiation or also on the
                      maintenance of the malignant state is unclear. Here, we show
                      that Atm reactivation in initially Atm-deficient B- and T
                      cell lymphomas induces tumor regression. We further find a
                      reduced T cell abundance in B cell lymphomas from
                      Atm-defective mice and A-T patients. Using T cell-specific
                      Atm-knockout models, as well as allogeneic transplantation
                      experiments, we pinpoint impaired immune surveillance as a
                      contributor to cancer predisposition and development.
                      Moreover, we demonstrate that Atm-deficient T cells display
                      impaired proliferation capacity upon stimulation, due to
                      replication stress. Altogether, our data indicate that T
                      cell-specific restoration of ATM activity or allogeneic
                      hematopoietic stem cell transplantation may prevent
                      lymphomagenesis in A-T patients.},
      keywords     = {Alleles / Animals / Ataxia Telangiectasia Mutated Proteins:
                      metabolism / Cell Proliferation / Etoposide: pharmacology /
                      Hematopoietic Stem Cell Transplantation / Lymphoma:
                      immunology / Lymphoma: metabolism / Mice / Mice, Knockout /
                      T-Lymphocytes: immunology / T-Lymphocytes: metabolism /
                      Transplantation, Homologous / Treatment Outcome},
      cin          = {AG Isbrandt},
      ddc          = {610},
      cid          = {I:(DE-2719)1011003},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31690822},
      doi          = {10.1038/s41375-019-0618-2},
      url          = {https://pub.dzne.de/record/145055},
}