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@ARTICLE{ErdreichEpstein:119911,
      author       = {A. Erdreich-Epstein and N. Robison and X. Ren and H. Zhou
                      and J. Xu and T. B. Davidson and M. Schur and F. H. Gilles
                      and L. Ji and J. Malvar and G. M. Shackleford and A. S.
                      Margol and M. D. Krieger and A. R. Judkins and D. Jones$^*$
                      and S. Pfister$^*$ and M. Kool$^*$ and R. Sposto and S.
                      Asgharzadeh and S. Asgharazadeh},
      title        = {{PID}1 ({NYGGF}4), a new growth-inhibitory gene in
                      embryonal brain tumors and gliomas.},
      journal      = {Clinical cancer research},
      volume       = {20},
      number       = {4},
      issn         = {1557-3265},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DKFZ-2017-00502},
      pages        = {827 - 836},
      year         = {2014},
      abstract     = {We present here the first report of PID1 (Phosphotyrosine
                      Interaction Domain containing 1; NYGGF4) in cancer. PID1 was
                      identified in 2006 as a gene that modulates insulin
                      signaling and mitochondrial function in adipocytes and
                      muscle cells.Using four independent medulloblastoma
                      datasets, we show that mean PID1 mRNA levels were lower in
                      unfavorable medulloblastomas (groups 3 and 4, and anaplastic
                      histology) compared with favorable medulloblastomas (SHH and
                      WNT groups, and desmoplastic/nodular histology) and with
                      fetal cerebellum. In two large independent glioma datasets,
                      PID1 mRNA was lower in glioblastomas (GBM), the most
                      malignant gliomas, compared with other astrocytomas,
                      oligodendrogliomas and nontumor brains. Neural and proneural
                      GBM subtypes had higher PID1 mRNA compared with classical
                      and mesenchymal GBM. Importantly, overall survival and
                      radiation-free progression-free survival were longer in
                      medulloblastoma patients whose tumors had higher PID1 mRNA
                      (univariate and multivariate analyses). Higher PID1 mRNA
                      also correlated with longer overall survival in patients
                      with glioma and GBM. In cell culture, overexpression of PID1
                      inhibited colony formation in medulloblastoma, atypical
                      teratoid rhabdoid tumor (ATRT), and GBM cell lines.
                      Increasing PID1 also increased cell death and apoptosis,
                      inhibited proliferation, induced mitochondrial
                      depolaization, and decreased serum-mediated phosphorylation
                      of AKT and ERK in medulloblastoma, ATRT, and/or GBM cell
                      lines, whereas siRNA to PID1 diminished mitochondrial
                      depolarization.These data are the first to link PID1 to
                      cancer and suggest that PID1 may have a tumor inhibitory
                      function in these pediatric and adult brain tumors.},
      keywords     = {Carrier Proteins (NLM Chemicals) / PID1 protein, human (NLM
                      Chemicals) / RNA, Messenger (NLM Chemicals)},
      cin          = {B062},
      ddc          = {610},
      cid          = {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:24300787},
      pmc          = {pmc:PMC3962776},
      doi          = {10.1158/1078-0432.CCR-13-2053},
      url          = {https://inrepo02.dkfz.de/record/119911},
}