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@ARTICLE{Tao:143394,
      author       = {R. Tao and N. Murad and Z. Xu and P. Zhang and K.
                      Okonechnikov$^*$ and M. Kool$^*$ and S. Rivero-Hinojosa and
                      C. Lazarski and P. Zheng and Y. Liu and C. G. Eberhart and
                      B. R. Rood and R. Packer and Y. Pei},
      title        = {{MYC} drives {G}roup 3 medulloblastoma through
                      transformation of {S}ox2+ astrocyte progenitor cells.},
      journal      = {Cancer research},
      volume       = {79},
      number       = {8},
      issn         = {1538-7445},
      address      = {Philadelphia, Pa.},
      publisher    = {AACR},
      reportid     = {DKFZ-2019-00982},
      pages        = {1967-1980},
      year         = {2019},
      note         = {;79(8):1967-1980},
      abstract     = {A subset of Group 3 medulloblastoma frequently harbors
                      amplification or overexpression of MYC lacking additional
                      focal aberrations, yet it remains unclear whether MYC
                      overexpression alone can induce tumorigenesis and which
                      cells give rise to these tumors. Here, we showed that
                      astrocyte progenitors in the early postnatal cerebellum were
                      susceptible to transformation by MYC. The resulting tumors
                      specifically resembled human Group 3 medulloblastoma based
                      on histology and gene expression profiling. Gene expression
                      analysis of MYC-driven medulloblastoma cells revealed
                      altered glucose metabolic pathways with marked
                      overexpression of lactate dehydrogenase A (LDHA). LDHA
                      abundance correlated positively with MYC expression and was
                      associated with poor prognosis in human Group 3
                      medulloblastoma. Inhibition of LDHA significantly reduced
                      growth of both mouse and human MYC-driven tumors but had
                      little effect on normal cerebellar cells or SHH-associated
                      medulloblastoma. By generating a new mouse model, we
                      demonstrated for the first time that astrocyte progenitors
                      can be transformed by MYC and serve as the cells of origin
                      for Group 3 medulloblastoma. Moreover, we identified LDHA as
                      a novel, specific therapeutic target for this devastating
                      disease.},
      cin          = {B062 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)L101-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30862721},
      doi          = {10.1158/0008-5472.CAN-18-1787},
      url          = {https://inrepo02.dkfz.de/record/143394},
}