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@ARTICLE{Schoof:307237,
      author       = {M. Schoof and T. Zheng$^*$ and M. Sill$^*$ and R. Imle$^*$
                      and A. Cais$^*$ and L. Altendorf and A. Fürst and N.
                      Hofmann$^*$ and K. Ernst$^*$ and D. Vonficht$^*$ and K. C.
                      Chan$^*$ and T. Holland-Letz$^*$ and A. Postlmayr and R.
                      Shiraishi and W. Wang and A. Morcavallo and M. Spohn and C.
                      Göbel and J. Niesen and L.-S. Peter and F. Bourdeaut and
                      Z.-Y. Han and Y. Pei and N. Murad and F. J. Swartling and J.
                      Taylor and M. Yadav and G. R. Gibson and R. J. Gilbertson
                      and M. Dottermusch and R. Roy and K. Kerl and R. Glass and
                      J. Cheng and M. A. Horstmann and G. Wolters-Eisfeld and H.
                      Zhao and D. Sturm$^*$ and V. N. Yadav and L. Chesler and S.
                      Haas and W. A. Weiss and P. A. Northcott and L. M.
                      Kutscher$^*$ and A. Guerreiro Stucklin and O. Ayrault and J.
                      E. Neumann and D. Kawauchi and D. Jones$^*$ and K.
                      Pajtler$^*$ and A. Banito$^*$ and S. Pfister$^*$ and U.
                      Schüller and M. Zuckermann$^*$},
      title        = {{I}nvestigation of a global mouse methylome atlas reveals
                      subtype-specific copy number alterations in pediatric cancer
                      models.},
      journal      = {Nature genetics},
      volume       = {nn},
      issn         = {1061-4036},
      address      = {London},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2025-02930},
      pages        = {nn},
      year         = {2025},
      note         = {#EA:B062#LA:B062# / epub/ DKFZ-ZMBH Alliance},
      abstract     = {Copy number alterations (CNAs) are hallmarks of cancer, yet
                      investigation of their oncogenic role has been hindered by
                      technical limitations and missing model systems. Here we
                      generated a genome-wide DNA methylation and CNA atlas of 106
                      genetic mouse models across 31 pediatric tumor types,
                      including 18 new models for pediatric glioma. We
                      demonstrated their epigenetic resemblance to human disease
                      counterparts and identified entity-specific patterns of
                      immune infiltration. We discovered that mouse tumors harbor
                      highly recurrent CNA signatures that occur distinctly based
                      on the tumor subgroup and driving oncogene and showed that
                      these CNAs share syntenic regions with the matching human
                      tumor types, thereby revealing a conserved but previously
                      underappreciated role in subgroup-specific tumorigenesis
                      that can be analyzed using the presented models. Our study
                      provides insights into globally available mouse models for
                      pediatric solid cancers and enables access to functional CNA
                      interrogation, with the potential to unlock new
                      translational targets in pediatric cancers.},
      cin          = {B062 / B360 / A010 / C060 / B430 / B380},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B360-20160331 /
                      I:(DE-He78)A010-20160331 / I:(DE-He78)C060-20160331 /
                      I:(DE-He78)B430-20160331 / I:(DE-He78)B380-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41381884},
      doi          = {10.1038/s41588-025-02419-4},
      url          = {https://inrepo02.dkfz.de/record/307237},
}