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@ARTICLE{Archer:137640,
      author       = {T. C. Archer and T. Ehrenberger and F. Mundt and M. P. Gold
                      and K. Krug and C. K. Mah and E. L. Mahoney and C. J. Daniel
                      and A. LeNail and D. Ramamoorthy and P. Mertins and D. R.
                      Mani and H. Zhang and M. A. Gillette and K. Clauser and M.
                      Noble and L. C. Tang and J. Pierre-François and J. Silterra
                      and J. Jensen and P. Tamayo and A. Korshunov$^*$ and S.
                      Pfister$^*$ and M. Kool$^*$ and P. A. Northcott$^*$ and R.
                      C. Sears and J. O. Lipton and S. A. Carr and J. P. Mesirov
                      and S. L. Pomeroy and E. Fraenkel},
      title        = {{P}roteomics, {P}ost-translational {M}odifications, and
                      {I}ntegrative {A}nalyses {R}eveal {M}olecular
                      {H}eterogeneity within {M}edulloblastoma {S}ubgroups.},
      journal      = {Cancer cell},
      volume       = {34},
      number       = {3},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2018-01520},
      pages        = {396 - 410.e8},
      year         = {2018},
      abstract     = {There is a pressing need to identify therapeutic targets in
                      tumors with low mutation rates such as the malignant
                      pediatric brain tumor medulloblastoma. To address this
                      challenge, we quantitatively profiled global proteomes and
                      phospho-proteomes of 45 medulloblastoma samples. Integrated
                      analyses revealed that tumors with similar RNA expression
                      vary extensively at the post-transcriptional and
                      post-translational levels. We identified distinct pathways
                      associated with two subsets of SHH tumors, and found
                      post-translational modifications of MYC that are associated
                      with poor outcomes in group 3 tumors. We found kinases
                      associated with subtypes and showed that inhibiting PRKDC
                      sensitizes MYC-driven cells to radiation. Our study shows
                      that proteomics enables a more comprehensive, functional
                      readout, providing a foundation for future therapeutic
                      strategies.},
      cin          = {G380 / B062 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)G380-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30205044},
      doi          = {10.1016/j.ccell.2018.08.004},
      url          = {https://inrepo02.dkfz.de/record/137640},
}