% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Brosus:210400,
      author       = {J. Broséus and S. Hergalant and J. Vogt and E. Tausch and
                      M. Kreuz and A. Mottok and C. Schneider and C. Dartigeas and
                      D. Roos-Weil and A. Quinquenel and C. Moulin and G. Ott and
                      O. Blanchet and C. Tomowiak and G. Lazarian and P. Rouyer
                      and E. Chteinberg and S. H. Bernhart and O. Tournilhac and
                      G. Gauchotte and S. Lomazzi and E. Chapiro and F.
                      Nguyen-Khac and C. Chery and F. Davi and M. Hunault and R.
                      Houlgatte and A. Rosenwald and A. Delmer and D. Meyre and
                      M.-C. Béné and C. Thieblemont and P. Lichter$^*$ and O.
                      Ammerpohl and J.-L. Guéant and R. Guièze and J. I.
                      Martin-Subero and F. Cymbalista and P. Feugier and R.
                      Siebert and S. Stilgenbauer},
      collaboration = {I. M. Consortium},
      othercontributors = {S. Bernhart},
      title        = {{M}olecular characterization of {R}ichter syndrome
                      identifies de novo diffuse large {B}-cell lymphomas with
                      poor prognosis.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00124},
      pages        = {309},
      year         = {2023},
      abstract     = {Richter syndrome (RS) is the transformation of chronic
                      lymphocytic leukemia (CLL) into aggressive lymphoma, most
                      commonly diffuse large B-cell lymphoma (DLBCL). We
                      characterize 58 primary human RS samples by genome-wide DNA
                      methylation and whole-transcriptome profiling. Our
                      comprehensive approach determines RS DNA methylation profile
                      and unravels a CLL epigenetic imprint, allowing CLL-RS
                      clonal relationship assessment without the need of the
                      initial CLL tumor DNA. DNA methylation- and
                      transcriptomic-based classifiers were developed, and testing
                      on landmark DLBCL datasets identifies a poor-prognosis,
                      activated B-cell-like DLBCL subset in 111/1772 samples. The
                      classification robustly identifies phenotypes very similar
                      to RS with a specific genomic profile, accounting for
                      $4.3-8.3\%$ of de novo DLBCLs. In this work, RS multi-omics
                      characterization determines oncogenic mechanisms,
                      establishes a surrogate marker for CLL-RS clonal
                      relationship, and provides a clinically relevant classifier
                      for a subset of primary 'RS-type DLBCL' with unfavorable
                      prognosis.},
      cin          = {B060 / HD01},
      ddc          = {500},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36658118},
      doi          = {10.1038/s41467-022-34642-6},
      url          = {https://inrepo02.dkfz.de/record/210400},
}