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@ARTICLE{Drr:132709,
      author       = {C. Dürr$^*$ and B. Hanna$^*$ and A. Schulz$^*$ and F.
                      Lucas$^*$ and M. Zucknick$^*$ and A. Benner$^*$ and A. Clear
                      and S. Ohl$^*$ and S. Öztürk$^*$ and T. Zenz$^*$ and S.
                      Stilgenbauer and M. Li-Weber$^*$ and P. Krammer$^*$ and J.
                      G. Gribben and P. Lichter$^*$ and M. Seiffert$^*$},
      title        = {{T}umor necrosis factor receptor signaling is a driver of
                      chronic lymphocytic leukemia that can be therapeutically
                      targeted by the flavonoid wogonin.},
      journal      = {Haematologica},
      volume       = {103},
      number       = {4},
      issn         = {1592-8721},
      address      = {Pavia},
      publisher    = {Ferrata Storti Foundation},
      reportid     = {DKFZ-2018-00363},
      pages        = {688 - 697},
      year         = {2018},
      abstract     = {Chronic lymphocytic leukemia is a malignancy of mature B
                      cells that strongly depend on microenvironmental factors,
                      and their deprivation has been identified as a promising
                      treatment approach for this incurable disease. Cytokine
                      array screening of 247 chronic lymphocytic leukemia serum
                      samples revealed elevated levels of tumor necrosis factor
                      (TNF) receptor-1 which were associated with poor clinical
                      outcome. We detected a microenvironment-induced expression
                      of TNF receptor-1 in chronic lymphocytic leukemia cells in
                      vitro, and an aberrantly high expression of this receptor in
                      the proliferation centers of patients' lymph nodes.
                      Stimulation of TNF receptor-1 with TNF-α enhanced nuclear
                      factor κ-light-chain-enhancer of activated B cells (NFκB)
                      activity and viability of chronic lymphocytic leukemia
                      cells, which was inhibited by wogonin. The therapeutic
                      effects of wogonin were analyzed in mice after adoptive
                      transfer of Eμ-T-cell leukemia 1 (TCL1) leukemic cells.
                      Wogonin treatment prevented leukemia development when given
                      early after transplantation. The treatment of full-blown
                      leukemia resulted in the loss of the TNF receptor-1 on
                      chronic lymphocytic leukemia cells and their mobilization to
                      blood. Targeting TNF receptor-1 signaling is therefore
                      proposed for the treatment of chronic lymphocytic leukemia.},
      cin          = {B060 / C060 / G100 / D030},
      ddc          = {610},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)G100-20160331 / I:(DE-He78)D030-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29326123},
      pmc          = {pmc:PMC5865430},
      doi          = {10.3324/haematol.2017.177808},
      url          = {https://inrepo02.dkfz.de/record/132709},
}