| Literature DB >> 29569163 |
Yojiro Akagi1, Koji Yoshimoto2, Nobuhiro Hata1, Daisuke Kuga1, Ryusuke Hatae1, Takeo Amemiya1, Yuhei Sangatsuda1, Satoshi O Suzuki3, Toru Iwaki3, Masahiro Mizoguchi4, Koji Iihara1.
Abstract
In this study, we reclassified 400 consecutive glioma cases including pediatric cases, using the revised 2016 WHO classification with samples collected from the Kyushu University Brain Tumor Bank. The IDH1/2, H3F3A, key genetic markers in the 2016 classification, were analyzed using high-resolution melting, with DNA extracted from frozen tissues. The 1p/19q codeletions were evaluated using a microsatellite-based loss of heterozygosity analysis, with 18 markers, to detect loss of the entire chromosome arm. In the integrated diagnosis, 29 oligodendroglioma cases and 28 anaplastic oligodendroglioma cases were diagnosed as "IDH-mutant and 1p/19q-codeleted," while 2 oligodendroglioma cases and 5 anaplastic oligodendroglioma cases were diagnosed as not otherwise specified (NOS). These "NOS" cases were either IDH-mutants or 1p/19q-codeleted, although characteristic oligodendroglial features were evident histologically. Better overall survival of patients with oligodendroglioma correlated with the molecular characteristic of "IDH-mutant and 1p/19q-codeleted," rather than the WHO grade. Eleven "glioblastoma, IDH-wild-type" cases were classified as "1p/19q-codeleted", however, chromosome 10 loss was also detected in 10 out of 11 cases. The 2016 WHO criteria for glioma classification leads to better diagnosis of patients. However, there are technical pitfalls and problems to be solved in the molecular analysis of routine diagnostics.Entities:
Keywords: Classification; Glioma; IDH; Molecular diagnosis; TERT; WHO
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Year: 2018 PMID: 29569163 DOI: 10.1007/s10014-018-0313-4
Source DB: PubMed Journal: Brain Tumor Pathol ISSN: 1433-7398 Impact factor: 3.298