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@ARTICLE{Bochtler:141915,
      author       = {T. Bochtler$^*$ and M. Merz and T. Hielscher$^*$ and M.
                      Granzow and K. Hoffmann and A. Krämer$^*$ and M.-S.
                      Raab$^*$ and J. Hillengass$^*$ and A. Seckinger and C.
                      Kimmich and T. Dittrich$^*$ and C. Müller-Tidow and D. Hose
                      and H. Goldschmidt$^*$ and U. Hegenbart and A. Jauch and S.
                      O. Schönland},
      title        = {{C}ytogenetic intraclonal heterogeneity of plasma cell
                      dyscrasia in {AL} amyloidosis as compared with multiple
                      myeloma.},
      journal      = {Blood advances},
      volume       = {2},
      number       = {20},
      issn         = {2473-9537},
      address      = {Washington, DC},
      publisher    = {American Society of Hematology},
      reportid     = {DKFZ-2018-02172},
      pages        = {2607 - 2618},
      year         = {2018},
      abstract     = {Analysis of intraclonal heterogeneity has yielded insights
                      into the clonal evolution of hematologic malignancies. We
                      compared the clonal and subclonal compositions of the
                      underlying plasma cell dyscrasia in 544 systemic light chain
                      amyloidosis (PC-AL) patients with 519 patients with
                      monoclonal gammopathy of undetermined significance (MGUS),
                      smoldering multiple myeloma (SMM), or symptomatic MM; ie,
                      PC-non-AL patients). Using interphase fluorescence in situ
                      hybridization, subclones were stringently defined as clone
                      size below two thirds of the largest clone and an absolute
                      difference of $≥30\%.$ Subclones were found less
                      frequently in the PC-AL group, at 199 $(36.6\%)$ of 544 as
                      compared with 267 $(51.4\%)$ of 519 in the PC-non-AL group
                      (P < .001), and were not associated with the stage of plasma
                      cell dyscrasia in either entity. In both groups,
                      translocation t(11;14), other immunoglobulin heavy chain
                      translocations, and hyperdiploidy were typically found as
                      main clones, whereas gain of 1q21 and deletions of 8p21,
                      13q14, and 17p13 were frequently found as subclones. There
                      were no shifts in the subclone/main clone ratio depending on
                      the MGUS, SMM, or MM stage of plasma cell dyscrasia. In
                      multivariate analysis, t(11;14) was associated with lower
                      rates of subclone formation and hyperdiploidy with higher
                      rates. PC-AL itself lost statistical significance,
                      demonstrating that the lower subclone frequency in AL is a
                      reflection of its exceptionally high t(11;14) frequency. In
                      summary, the subclone patterns in PC-AL and PC-non-AL are
                      closely related, implying that subclone formation depends on
                      the main cytogenetic categories and is independent of
                      disease entity and stage.},
      cin          = {G330 / C060},
      ddc          = {610},
      cid          = {I:(DE-He78)G330-20160331 / I:(DE-He78)C060-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30327369},
      pmc          = {pmc:PMC6199662},
      doi          = {10.1182/bloodadvances.2018023200},
      url          = {https://inrepo02.dkfz.de/record/141915},
}