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@ARTICLE{Dubois:180591,
      author       = {F. P. B. Dubois and O. Shapira and N. F. Greenwald and T.
                      Zack and J. Wala and J. W. Tsai and A. Crane and A. Baguette
                      and D. Hadjadj and A. S. Harutyunyan and K. H. Kumar and M.
                      Blattner-Johnson$^*$ and J. Vogelzang and C. Sousa and K. S.
                      Kang and C. Sinai and D. K. Wang and P. Khadka and K. Lewis
                      and L. Nguyen and H. Malkin and P. Ho and R. O'Rourke and S.
                      Zhang and R. Gold and D. Deng and J. Serrano and M. Snuderl
                      and C. Jones and K. D. Wright and S. N. Chi and J. Grill and
                      C. L. Kleinman and L. C. Goumnerova and N. Jabado and D.
                      Jones$^*$ and M. W. Kieran and K. L. Ligon and R. Beroukhim
                      and P. Bandopadhayay},
      title        = {{S}tructural variants shape driver combinations and
                      outcomes in pediatric high-grade glioma.},
      journal      = {Nature cancer},
      volume       = {3},
      number       = {8},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2022-01425},
      pages        = {994-1011},
      year         = {2022},
      note         = {2022 Aug;3(8):994-1011},
      abstract     = {We analyzed the contributions of structural variants (SVs)
                      to gliomagenesis across 179 pediatric high-grade gliomas
                      (pHGGs). The most recurrent SVs targeted MYC isoforms and
                      receptor tyrosine kinases (RTKs), including an SV amplifying
                      a MYC enhancer in $12\%$ of diffuse midline gliomas (DMG),
                      indicating an underappreciated role for MYC in pHGG. SV
                      signature analysis revealed that tumors with simple
                      signatures were TP53 wild type (TP53WT) but showed
                      alterations in TP53 pathway members PPM1D and MDM4. Complex
                      signatures were associated with direct aberrations in TP53,
                      CDKN2A and RB1 early in tumor evolution and with
                      later-occurring extrachromosomal amplicons. All pHGGs
                      exhibited at least one simple-SV signature, but complex-SV
                      signatures were primarily restricted to subsets of H3.3K27M
                      DMGs and hemispheric pHGGs. Importantly, DMGs with
                      complex-SV signatures were associated with shorter overall
                      survival independent of histone mutation and TP53 status.
                      These data provide insight into the impact of SVs on
                      gliomagenesis and the mechanisms that shape them.},
      cin          = {B360 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B360-20160331 / 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:35788723},
      doi          = {10.1038/s43018-022-00403-z},
      url          = {https://inrepo02.dkfz.de/record/180591},
}