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@ARTICLE{Berg:301538,
      author       = {V. Berg and A. Lollies and M. Schneider and P. Johansson
                      and M. A. Weniger and E. Albertini and F. Facchetti and S.
                      Ascani and A. Moawia and S. Bens and A. Fischer and R.
                      Siebert and W. Klapper and L. Lorenzi and E. Tiacci and S.
                      Hartmann and B. Budeus and M.-L. Hansmann and R.
                      Küppers$^*$},
      title        = {{C}ommon origin and somatic mutation patterns of composite
                      lymphomas and leukemias.},
      journal      = {Leukemia},
      volume       = {39},
      number       = {8},
      issn         = {0887-6924},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2025-01059},
      pages        = {1960-1971},
      year         = {2025},
      note         = {2025 Aug;39(8):1960-1971},
      abstract     = {When two lymphomas occur concurrently or sequentially in a
                      patient, it is a major question whether they derive from the
                      same lymphocyte or hematopoietic precursor cell or developed
                      independently. We studied four composite classic Hodgkin
                      lymphomas (HL) and other mature B-cell lymphomas, and two
                      composite mature B- and T-cell neoplasias by whole exome
                      sequencing (WES). Analysis of their IGV genes revealed that
                      three composite B-cell lymphomas originated from common
                      germinal center-experienced B cells. WES identified shared
                      somatic mutations in the lymphomas of these clonally related
                      composite lymphomas, indicating their derivation from a
                      common, pre-malignant precursor. Most mutations were
                      restricted to one or the other of these lymphomas, likely
                      explaining how distinct lymphomas developed from a common
                      ancestral B cell. In the two B-cell/T-cell lymphoma cases,
                      and a composite clonally unrelated HL/chronic lymphocytic
                      leukemia, the lymphoma partners did not share any somatic
                      mutations. In three cases, we identified potentially
                      oncogenic variants also in cells serving as constitutional
                      controls. These variants may have contributed to development
                      of a composite lymphoma/leukemia. We provide additional
                      evidence of frequent clonal relation in composite lymphomas,
                      highlight the multistep transformation process of related
                      lymphomas with a likely pre-malignant intermediate common
                      precursor, and support the importance of constitutional
                      variants in lymphomagenesis.},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40404986},
      doi          = {10.1038/s41375-025-02549-y},
      url          = {https://inrepo02.dkfz.de/record/301538},
}