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@ARTICLE{Mille:119945,
      author       = {F. Mille and L. Tamayo-Orrego and M. Lévesque and M. Remke
                      and A. Korshunov$^*$ and J. Cardin and N. Bouchard and L.
                      Izzi and M. Kool$^*$ and P. A. Northcott$^*$ and M. D.
                      Taylor and S. Pfister$^*$ and F. Charron},
      title        = {{T}he {S}hh receptor {B}oc promotes progression of early
                      medulloblastoma to advanced tumors.},
      journal      = {Developmental cell},
      volume       = {31},
      number       = {1},
      issn         = {1534-5807},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-00536},
      pages        = {34 - 47},
      year         = {2014},
      abstract     = {During cerebellar development, Sonic hedgehog (Shh)
                      signaling drives the proliferation of granule cell
                      precursors (GCPs). Aberrant activation of Shh signaling
                      causes overproliferation of GCPs, leading to
                      medulloblastoma. Although the Shh-binding protein Boc
                      associates with the Shh receptor Ptch1 to mediate Shh
                      signaling, whether Boc plays a role in medulloblastoma is
                      unknown. Here, we show that BOC is upregulated in
                      medulloblastomas and induces GCP proliferation. Conversely,
                      Boc inactivation reduces proliferation and progression of
                      early medulloblastomas to advanced tumors. Mechanistically,
                      we find that Boc, through elevated Shh signaling, promotes
                      high levels of DNA damage, an effect mediated by CyclinD1.
                      High DNA damage in the presence of Boc increases the
                      incidence of Ptch1 loss of heterozygosity, an important
                      event in the progression from early to advanced
                      medulloblastoma. Together, our results indicate that DNA
                      damage promoted by Boc leads to the demise of its own
                      coreceptor, Ptch1, and consequently medulloblastoma
                      progression.},
      keywords     = {Boc protein, mouse (NLM Chemicals) / Hedgehog Proteins (NLM
                      Chemicals) / Immunoglobulin G (NLM Chemicals) / PTCH
                      protein, human (NLM Chemicals) / Patched Receptors (NLM
                      Chemicals) / Patched-1 Receptor (NLM Chemicals) / Ptch1
                      protein, mouse (NLM Chemicals) / Receptors, Cell Surface
                      (NLM Chemicals) / Shh protein, mouse (NLM Chemicals) /
                      Cyclin D1 (NLM Chemicals)},
      cin          = {G380 / B062},
      ddc          = {570},
      cid          = {I:(DE-He78)G380-20160331 / I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25263791},
      doi          = {10.1016/j.devcel.2014.08.010},
      url          = {https://inrepo02.dkfz.de/record/119945},
}