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@ARTICLE{Rausch:302990,
      author       = {T. Rausch and H. Schäfer and J. Bein and F. Mölder and L.
                      K. Beeck and B. Kölsch and S. Borchert and V. Benes and T.
                      Halbsguth and U. Brunnberg and T. Oellerich$^*$ and T.
                      Tousseyn and M. Ponzoni and J. Köster and M.-L. Hansmann
                      and R. Küppers$^*$ and S. Hartmann},
      title        = {{G}enetic lesions in nodular lymphocyte-predominant
                      {H}odgkin lymphoma and {T} cell/histiocyte-rich large
                      {B}-cell lymphoma identified by whole genome sequencing.},
      journal      = {Leukemia},
      volume       = {39},
      number       = {9},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01437},
      pages        = {2215-2225},
      year         = {2025},
      note         = {2025 Sep;39(9):2215-2225},
      abstract     = {Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) is
                      a rare malignant lymphoma characterised by a few large
                      tumour cells expressing B-cell antigens in an inflammatory
                      background. T-cell/histiocyte-rich large B-cell lymphoma
                      (THRLBCL) is now considered to be closely related to NLPHL.
                      Little is known about the mutational spectrum of the
                      lymphoma cells in primary NLPHL and THRLBCL due to the
                      rarity of the diseases and the technical challenges of
                      analysing these tumours. Therefore, the aim of the present
                      study was to elucidate mechanisms contributing to the
                      pathogenesis of NLPHL and THRLBCL by whole genome sequencing
                      of laser microdissected tumour cells from seven cases. We
                      observed a heterogeneity of transforming events, with cases
                      showing abundant somatic mutations, others with a
                      predominance of structural variations, and cases with few
                      aberrations. The genes that were most frequently affected by
                      aberrations encode factors influencing JAK-STAT, NF-κB,
                      and/or WNT signaling, and apoptosis regulators. However, the
                      mutated genes, such as SOCS3, JUNB, IRF1 and ITPKB, were not
                      the typical targets known from classical Hodgkin lymphoma
                      (cHL). Two cases showed recurrent rearrangements of BCL6 and
                      CD74. In conclusion, our data enrich our understanding of
                      NLPHL and THRLBCL and highlight common and distinct features
                      with respect to cHL.},
      cin          = {FM01 / ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331 / I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40670673},
      doi          = {10.1038/s41375-025-02679-3},
      url          = {https://inrepo02.dkfz.de/record/302990},
}