Integrated molecular genetic profiling of pediatric high-grade gliomas reveals key differences with the adult disease.

By Barbara S. Paugh, Chunxu Qu, Chris Jones, Zhaoli Liu, M. Adamowicz-Brice, Junyuan Zhang, D. Bax, B. Coyle, Jennifer Barrow, D. Hargrave and 7 more. Journal of Clinical Oncology, 2010

607 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/743aba086f8c5f2779e0553697d61ee22b200948

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In Genetics

1. Vladimir Lazar
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Citations in the corpus

• Glioblastoma: pathology, molecular mechanisms and markers (2015, background): “For example, in a fraction of anaplastic gliomas and particularly in GBMs, the CDKN2A gene is homozygously deleted; CDKN2A locus encodes both Ink4A and Arf proteins, which are crucial activators of Rb and p53, respectively [22, 123, 126, 163].”
• Mesenchymal Transition and PDGFRA Amplification/Mutation Are Key Distinct Oncogenic Events in Pediatric Diffuse Intrinsic Pontine Gliomas (2012, background): “PDGFRA amplification has been shown to be more frequent in pediatric HGG than in adult ones [8] and a recent report found PDGFRA gain or amplification in four out of eleven post-mortem samples of DIPG [10].”
• K27M mutation in histone H3.3 defines clinically and biologically distinct subgroups of pediatric diffuse intrinsic pontine gliomas (2012, background): “21 (q = 0.033) corresponding to PDGFRA and MYC/PVT1 locus gains/amplifications, respectively (Fig.”
• Integrated Molecular Meta-Analysis of 1,000 Pediatric High-Grade and Diffuse Intrinsic Pontine Glioma (2017, background): “…2014; Grasso et al., 2015; International Cancer Genome Consortium PedBrain Tumor Project, 2016; Khuong-Quang et al., 2012; Korshunov et al., 2015; Paugh et al., 2010, 2011; Puget et al., 2012; Schwartzentruber et al., 2012; Sturm et al., 2012; Taylor et al., 2014a; Wu et al., 2012; Wu et al.,…”
• Hotspot mutations in H3F3A and IDH1 define distinct epigenetic and biological subgroups of glioblastoma. (2012, methodology): “Furthermore, IDH1 or IDH2 mutations, which are found in up to 98% of adult secondary GBM, are very rare in childhood GBM (<10%) (Antonelli et al., 2010; Balss et al., 2008; De Carli et al., 2009; Paugh et al., 2010; Pollack et al., 2011; Schiffman et al., 2010; Setty et al., 2010; Yan et al., 2009).”