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@ARTICLE{Lehners:142466,
      author       = {N. Lehners$^*$ and E. Ellert and J. Xu$^*$ and J.
                      Hillengass and J. Leichsenring and A. Stenzinger and H.
                      Goldschmidt and M. Andrulis and M.-S. Raab$^*$},
      title        = {{O}ncogene-induced senescence: a potential breakpoint
                      mechanism against malignant transformation in plasma cell
                      disorders.},
      journal      = {Leukemia and lymphoma},
      volume       = {59},
      number       = {11},
      issn         = {1029-2403},
      address      = {London [u.a.]},
      publisher    = {Taylor $\&$ Francis Group},
      reportid     = {DKFZ-2019-00185},
      pages        = {2660 - 2669},
      year         = {2018},
      abstract     = {Oncogene-induced senescence (OIS) is a cellular
                      tumor-suppressive mechanism present in several premalignant
                      conditions. Here, we analyze the possible impact of OIS on
                      malignant transformation in plasma cell disorders. Tumor
                      samples from 125 patients with different disease stages were
                      analyzed immunohistochemically for expression of senescence
                      markers. Protein expression of cyclin-dependent kinase
                      inhibitor p21Cip1/Waf1 was significantly higher in
                      smoldering multiple myeloma (SMM) compared to monoclonal
                      gammopathy of undetermined significance (MGUS) (p = .02)
                      or symptomatic multiple myeloma (MM) (p = .005). SMM
                      plasma cells expressing p21Cip1/Waf1 were negative for Ki67,
                      consistent with senescence. While p27Kip1 was highly
                      expressed in healthy controls, MGUS and SMM, expression
                      decreased significantly in MM (p = .02). SMM plasma
                      cells displayed a mutually exclusive expression of
                      p21Cip1/Waf1/p27Kip1 suggesting compensatory mechanisms of
                      senescence. In conclusion, we found markers of cellular
                      senescence differentially expressed in SMM compared to MGUS
                      and MM supporting the hypothesis of OIS as a breakpoint
                      mechanism against malignant transformation in plasma cell
                      disorders.},
      cin          = {G170},
      ddc          = {610},
      cid          = {I:(DE-He78)G170-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29616856},
      doi          = {10.1080/10428194.2018.1443450},
      url          = {https://inrepo02.dkfz.de/record/142466},
}