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@ARTICLE{Lipka:131643,
      author       = {D. B. Lipka$^*$ and T. Witte$^*$ and R. Toth$^*$ and J.
                      Yang$^*$ and M. Wiesenfarth$^*$ and P. Nöllke and A.
                      Fischer and D. Brocks$^*$ and Z. Gu$^*$ and J. Park$^*$ and
                      B. Strahm and M. Wlodarski and A. Yoshimi and R. Claus and
                      M. Lübbert and H. Busch and M. Boerries and M. Hartmann$^*$
                      and M. Schönung$^*$ and U. Kilik$^*$ and J. Langstein$^*$
                      and J. A. Wierzbinska$^*$ and C. Pabst and S. Garg and A.
                      Catalá and B. De Moerloose and M. Dworzak and H. Hasle and
                      F. Locatelli and R. Masetti and M. Schmugge and O. Smith and
                      J. Stary and M. Ussowicz and M. M. van den Heuvel-Eibrink
                      and Y. Assenov$^*$ and M. Schlesner$^*$ and C. Niemeyer and
                      C. Flotho and C. Plass},
      title        = {{RAS}-pathway mutation patterns define epigenetic
                      subclasses in juvenile myelomonocytic leukemia.},
      journal      = {Nature Communications},
      volume       = {8},
      number       = {1},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-06275},
      pages        = {2126},
      year         = {2017},
      note         = {(* Co-first authors)},
      abstract     = {Juvenile myelomonocytic leukemia (JMML) is an aggressive
                      myeloproliferative disorder of early childhood characterized
                      by mutations activating RAS signaling. Established clinical
                      and genetic markers fail to fully recapitulate the clinical
                      and biological heterogeneity of this disease. Here we report
                      DNA methylome analysis and mutation profiling of 167 JMML
                      samples. We identify three JMML subgroups with unique
                      molecular and clinical characteristics. The high methylation
                      group (HM) is characterized by somatic PTPN11 mutations and
                      poor clinical outcome. The low methylation group is enriched
                      for somatic NRAS and CBL mutations, as well as for Noonan
                      patients, and has a good prognosis. The intermediate
                      methylation group (IM) shows enrichment for monosomy 7 and
                      somatic KRAS mutations. Hypermethylation is associated with
                      repressed chromatin, genes regulated by RAS signaling,
                      frequent co-occurrence of RAS pathway mutations and
                      upregulation of DNMT1 and DNMT3B, suggesting a link between
                      activation of the DNA methylation machinery and mutational
                      patterns in JMML.},
      cin          = {C010 / B080 / B240 / C060 / L601 / L101},
      ddc          = {500},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)B080-20160331 /
                      I:(DE-He78)B240-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)L601-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {313 - Cancer risk factors and prevention (POF3-313)},
      pid          = {G:(DE-HGF)POF3-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29259247},
      pmc          = {pmc:PMC5736667},
      doi          = {10.1038/s41467-017-02177-w},
      url          = {https://inrepo02.dkfz.de/record/131643},
}