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@ARTICLE{Scherger:144514,
      author       = {A. K. Scherger and M. Al-Maarri and H. C. Maurer and M.
                      Schick and S. Maurer and R. Öllinger and I.
                      Gonzalez-Menendez and M. Martella and M. Thaler and K.
                      Pechloff$^*$ and K. Steiger$^*$ and S. Sander$^*$ and J.
                      Ruland$^*$ and R. Rad$^*$ and L. Quintanilla-Martinez and F.
                      T. Wunderlich and S. Rose-John and U. Keller$^*$},
      title        = {{A}ctivated gp130 signaling selectively targets {B} cell
                      differentiation to induce mature lymphoma and plasmacytoma.},
      journal      = {JCI insight},
      volume       = {4},
      number       = {15},
      issn         = {2379-3708},
      address      = {Ann Arbor, Michigan},
      publisher    = {JCI Insight},
      reportid     = {DKFZ-2019-01962},
      pages        = {e128435},
      year         = {2019},
      abstract     = {Aberrant activity of the glycoprotein 130 130/JAK/STAT3
                      (gp130/JAK/STAT3) signaling axis is a recurrent event in
                      inflammation and cancer. In particular, it is associated
                      with a wide range of hematological malignancies, including
                      multiple myeloma and leukemia. Novel targeted therapies have
                      only been successful for some subtypes of these
                      malignancies, underlining the need for developing robust
                      mouse models to better dissect the role of this pathway in
                      specific tumorigenic processes. Here, we investigated the
                      role of selective gp130/JAK/STAT3 activation by generating a
                      conditional mouse model. This model targeted constitutively
                      active, cell-autonomous gp130 activity to B cells, as well
                      as to the entire hematopoietic system. We found that
                      regardless of the timing of activation in B cells,
                      constitutively active gp130 signaling resulted in the
                      formation specifically of mature B cell lymphomas and plasma
                      cell disorders with full penetrance, only with different
                      latencies, where infiltrating CD138+ cells were a dominant
                      feature in every tumor. Furthermore, constitutively active
                      gp130 signaling in all adult hematopoietic cells also led to
                      the development specifically of largely mature, aggressive B
                      cell cancers, again with a high penetrance of CD138+ tumors.
                      Importantly, gp130 activity abrogated the differentiation
                      block induced by a B cell-targeted Myc transgene and
                      resulted in a complete penetrance of the gp130-associated,
                      CD138+, mature B cell lymphoma phenotype. Thus, gp130
                      signaling selectively provides a strong growth and
                      differentiation advantage for mature B cells and directs
                      lymphomagenesis specifically toward terminally
                      differentiated B cell cancers.},
      cin          = {D180 / L701},
      ddc          = {610},
      cid          = {I:(DE-He78)D180-20160331 / I:(DE-He78)L701-20160331},
      pnm          = {314 - Tumor immunology (POF3-314)},
      pid          = {G:(DE-HGF)POF3-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31391340},
      doi          = {10.1172/jci.insight.128435},
      url          = {https://inrepo02.dkfz.de/record/144514},
}