1 Ocak 2016 Dergi makalesi Açık Erişim

Oktay, Yavuz; Ulgen, Ege; Can, Ozge; Akyerli, Cemaliye B.; Yuksel, Sirin; Erdemgil, Yigit; Durasi, I. Melis; Henegariu, Octavian Ioan; Nanni, E. Paolo; Selevsek, Nathalie; Grossmann, Jonas; Erson-Omay, E. Zeynep; Bai, Hanwen; Gupta, Manu; Lee, William; Turcan, Sevin; Ozpinar, Aysel; Huse, Jason T.; Sav, M. Aydin; Flanagan, Adrienne; Flanagan, Adrienne

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{
  "@context": "https://schema.org/", 
  "@id": 59661, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "name": "Oktay, Yavuz"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Acibadem Univ, Brain Tumor Res Grp, Istanbul, Turkey", 
      "name": "Ulgen, Ege"
    }, 
    {
      "@type": "Person", 
      "name": "Can, Ozge"
    }, 
    {
      "@type": "Person", 
      "name": "Akyerli, Cemaliye B."
    }, 
    {
      "@type": "Person", 
      "name": "Yuksel, Sirin"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Acibadem Univ, Brain Tumor Res Grp, Istanbul, Turkey", 
      "name": "Erdemgil, Yigit"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Sabanci Univ, Fac Engn & Nat Sci, Dept Biol Sci & Bioengn, Istanbul, Turkey", 
      "name": "Durasi, I. Melis"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT 06504 USA", 
      "name": "Henegariu, Octavian Ioan"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UZH ETH, Funct Genom Ctr Zurich, Zurich, Switzerland", 
      "name": "Nanni, E. Paolo"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UZH ETH, Funct Genom Ctr Zurich, Zurich, Switzerland", 
      "name": "Selevsek, Nathalie"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UZH ETH, Funct Genom Ctr Zurich, Zurich, Switzerland", 
      "name": "Grossmann, Jonas"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT 06504 USA", 
      "name": "Erson-Omay, E. Zeynep"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT 06504 USA", 
      "name": "Bai, Hanwen"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, Canc Inst, 72 Huntley St, London WC1E 6DD, England", 
      "name": "Gupta, Manu"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Mem Sloan Kettering Canc Ctr, Dept Radiat Oncol, New York, NY 10065 USA", 
      "name": "Lee, William"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York, NY 10065 USA", 
      "name": "Turcan, Sevin"
    }, 
    {
      "@type": "Person", 
      "name": "Ozpinar, Aysel"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10065 USA", 
      "name": "Huse, Jason T."
    }, 
    {
      "@type": "Person", 
      "name": "Sav, M. Aydin"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, Canc Inst, 72 Huntley St, London WC1E 6DD, England", 
      "name": "Flanagan, Adrienne"
    }, 
    {
      "@type": "Person", 
      "affiliation": "UCL, Canc Inst, 72 Huntley St, London WC1E 6DD, England", 
      "name": "Flanagan, Adrienne"
    }
  ], 
  "datePublished": "2016-01-01", 
  "description": "The single nucleotide polymorphism rs55705857, located in a non-coding but evolutionarily conserved region at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a causal variant. However, the molecular mechanism underlying this association has remained unknown. With a case control study in 285 gliomas, 316 healthy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we identified that the association was specific to IDH-mutant gliomas. Odds-ratios were 9.25 (5.17-16.52; 95% CI) for IDH-mutated gliomas and 12.85 (5.94-27.83; 95% CI) for IDH-mutated, 1p/19q co-deleted gliomas. Decreasing strength with increasing anaplasia implied a modulatory effect. No somatic mutations were noted at this locus in 114 blood-tumor pairs, nor was there a copy number difference between risk-allele and only-ancestral allele carriers. CCDC26 RNA-expression was rare and not different between the two groups. There were only minor subtype-specific differences in common glioma driver genes. RNA sequencing and LC-MS/MS comparisons pointed to significantly altered MYC-signaling. Baseline enhancer activity of the conserved region specifically on the MYC promoter and its further positive modulation by the SNP risk-allele was shown in vitro. Our findings implicate MYC deregulation as the underlying cause of the observed association.", 
  "headline": "IDH-mutant glioma specific association of rs55705857 located at 8q24.21 involves MYC deregulation", 
  "identifier": 59661, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "IDH-mutant glioma specific association of rs55705857 located at 8q24.21 involves MYC deregulation", 
  "url": "https://aperta.ulakbim.gov.tr/record/59661"
}