case_images: PMC7270112_01
case_images: Radiological and histological features of a 30-year-old glioneuronal tumor (GNT) case.. a Magnetic resonance images show multi-cystic mass in left parietal lobe with peritumoral edema. Scanty enhancement is observed in the solid portion of the mass. No calcification is identified in the computed tomography. b The tumor shows well-developed blood vessels with perivascular hyalinization with sheet of tumor cells between the blood vessels (H&E bar: 200 mum). Atypical hyperchromatic or multiple nuclei are observed, which are possibly degenerative atypia produced by long-standing slow growing nature of the tumor (H&E bar: 100 mum). Immunohistochemical studies reveal positive tumor cell nuclei for NeuN antibody (bar 200 mum), diffuse strong positivity in tumor cells for synaptophysin (bar 200 mum), focal positivity for Olig2 (bar: 100 mum), focal positivity for GFAP (100 mum), diffuse positivity for c-MET (bar: 100 mum), and low Ki67 labeling index of 0.4% (bar: 100 mum).
case_images: 41525_2020_131_Fig1_HTML.jpg
case_images: PMC7270112_01_41525_2020_131_Fig1_HTML.jpg
case_images: Fig1
case_images: Magnetic resonance images (MRI) showed a mixed solid and cystic mass in the left parietal lobe (Fig. 1a). The histological diagnosis using immunohistochemistry (IHC) studies was compatible with GNT (Fig. 1b). SMO, EZH2 which were annotated in COSMIC, the catalog of somatic mutations in cancer (Fig. 3, Supplementary Data Set 1). Somatic mutations from WES analysis were filtered with 1000 g, ExAC, gnomAD (allele frequency < 0.01) databases focusing on the exonic and splicing regions.
case_images: Copy number abnormalities and somatic mutations in the reported case of glioneuronal tumor (GNT).. Both chromosomes 1 and 7 shows a significant amount of copy number gains and losses compared to the other chromosomes.
case_images: 41525_2020_131_Fig3_HTML.jpg
case_images: PMC7270112_01_41525_2020_131_Fig3_HTML.jpg
case_images: Fig3
case_images: SMO, EZH2 which were annotated in COSMIC, the catalog of somatic mutations in cancer (Fig. 3, Supplementary Data Set 1). Somatic mutations from WES analysis were filtered with 1000 g, ExAC, gnomAD (allele frequency < 0.01) databases focusing on the exonic and splicing regions.