% 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{Schoof:285654,
      author       = {M. Schoof and S. Godbole and T. K. Albert and M.
                      Dottermusch and C. Walter and A. Ballast and N. Qin$^*$ and
                      M. B. Olivera$^*$ and C. Göbel and S. Neyazi and D. Holdhof
                      and C. Kresbach and L.-S. Peter and G. D. Epplen and V.
                      Thaden and M. Spohn and M. Blattner-Johnson$^*$ and F.
                      Modemann and M. Mynarek and S. Rutkowski and M. Sill$^*$ and
                      J. Varghese and A.-K. Afflerbach and A. Eckhardt and D.
                      Münter and A. Verma and N. Struve and D. Jones$^*$ and M.
                      Remke$^*$ and J. E. Neumann and K. Kerl and U. Schüller},
      title        = {{M}ouse models of pediatric high-grade gliomas with {MYCN}
                      amplification reveal intratumoral heterogeneity and lineage
                      signatures.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-02477},
      pages        = {7717},
      year         = {2023},
      abstract     = {Pediatric high-grade gliomas of the subclass MYCN
                      (HGG-MYCN) are highly aggressive tumors frequently carrying
                      MYCN amplifications, TP53 mutations, or both alterations.
                      Due to their rarity, such tumors have only recently been
                      identified as a distinct entity, and biological as well as
                      clinical characteristics have not been addressed
                      specifically. To gain insights into tumorigenesis and
                      molecular profiles of these tumors, and to ultimately
                      suggest alternative treatment options, we generated a
                      genetically engineered mouse model by breeding
                      hGFAP-cre::Trp53Fl/Fl::lsl-MYCN mice. All mice developed
                      aggressive forebrain tumors early in their lifetime that
                      mimic human HGG-MYCN regarding histology, DNA methylation,
                      and gene expression. Single-cell RNA sequencing revealed a
                      high intratumoral heterogeneity with neuronal and
                      oligodendroglial lineage signatures. High-throughput drug
                      screening using both mouse and human tumor cells finally
                      indicated high efficacy of Doxorubicin, Irinotecan, and
                      Etoposide as possible therapy options that children with
                      HGG-MYCN might benefit from.},
      keywords     = {Humans / Child / Mice / Animals / N-Myc Proto-Oncogene
                      Protein: genetics / N-Myc Proto-Oncogene Protein: metabolism
                      / Neuroblastoma: metabolism / Disease Models, Animal /
                      Glioma: genetics / Mutation / Gene Amplification / N-Myc
                      Proto-Oncogene Protein (NLM Chemicals) / MYCN protein, human
                      (NLM Chemicals)},
      cin          = {B360 / B062 / HD01 / ED01},
      ddc          = {500},
      cid          = {I:(DE-He78)B360-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)ED01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38001143},
      pmc          = {pmc:PMC10673884},
      doi          = {10.1038/s41467-023-43564-w},
      url          = {https://inrepo02.dkfz.de/record/285654},
}