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  1. 1

    المصدر: Neuropathology. 40:599-605

    الوصف: Glioma is the most common intracranial malignant tumor, with poor prognosis. The new World Health Organization (WHO) integrated classification (2016) for diffuse glioma is mainly based on the status of the isocitrate dehydrogenase (IDH) gene (IDH) mutation and 1p/19q codeletion, with diffuse glioma separated into three distinct molecular categories: chromosome 1p/19q codeletion/IDH mutant, 1p/19q intact /IDH mutant, and IDH wild-type. Gliomas harboring 1p/19q codeletion but without IDH mutation are rare and cannot be classified according to the new revision of the WHO classification. Here we report three high-grade gliomas with this atypical molecular phenotype, and describe their histological and immunohistochemical features, the status of mutations in TERT promopter, H3F3A, HIST1H3B, and BRAF, as well as MGMT promoter methylation, and prognosis. Considering morphology, molecular parameters, and patients prognosis, we found that high-grade gliomas harboring 1p/19q codeletion but without IDH mutation were not typical glioblastoma multiforme (GBM) but were more likely to be GBM than anaplastic oligodendroglioma.

  2. 2

    المصدر: Neuropathology. 29:156-165

    الوصف: Prostaglandin E2 has been connected to processes promoting tumor growth in several human malignancies including gliomas. The terminal prostaglandin synthases mPGES-1, mPGES-2, and cPGES convert PGH2 into prostaglandin E2. The inhibition of their function could significantly reduce PGE2 levels in tumors while avoiding some side effects related to the inhibition of the upstream enzymes COX-1 and COX-2. In this study, the immunohistochemical staining of mPGES-1 and, for the first time, the staining of mPGES-2 and cPGES are characterized and compared with COX-1 and COX-2 staining in the same tumor samples of 94 human gliomas. The main results demonstrate over-expression of all three proteins, including cPGES and mPGES-2 that are commonly considered non-inducible, in both low- and high-grade tumors. For all three proteins, average expression in tumor cells was higher in grade III tumors than grade II tumors. The analysis showed no correlation between tumor grade and staining of tumor cells or vascular endothelium with any of the antibodies except in oligodendrogliomas where moderate correlation (linear correlation coefficient 0.6; P

  3. 3

    المصدر: Neuropathology. 27:10-20

    الوصف: To verify the prognostic implications of the statuses of chromosome 1p and 19q and the expressions of p53, p16 and GFAP in oligodendrogliomas, we investigated these parameters and correlated the results with patient outcome. Twenty-seven cases of low-grade oligodendroglioma (LO) and 29 cases of anaplastic oligodendroglioma (AO) were analyzed by FISH for 1p and 19q status and by immunohistochemistry for p53, p16, and GFAP expression using a tissue microarray. Direct sequencing of the p53 gene was also performed. 1p deletion was observed in 39 of 56 patients (69.9%), and 19q deletion in 41 of 56 (73.2%). Combined loss of 1p and 19q was found in 38 of 56 (67.9%) and exhibited distinct concomitant deletion (P = 0.000). p53 overexpression was observed in 17 cases (30.3%), GFAP expression in 18 cases (32.1%), and p16 loss in 40 cases (74%) of oligodendrogliomas. The expressions of p53 and GFAP were more frequent in AO than in LO (P= 0.015 and 0.001). In contrast, p53 expression was more common in oligodendrogliomas with an intact 19q (P= 0.029), or an intact 1p (P= 0.071). Only five of 14 patients with p53 expression showed TP53 mutation, which was inversely correlated with 1p deletion (P= 0.036). Patients with combined loss of 1p and 19q exhibited better overall survival (P = 0.045). Patients with p53 expression without combined 1p and 19q loss showed poor overall survival (P0.000). However, TP53 mutation along with 1p and 19q status could not predict patient outcome. Patients with p16 loss without combined 1p and 9q loss showed poor overall survival (P = 0.011). Therefore, in oligodendrogliomas, the absence of the combined deletion of 1p and 19q and the aberrant expression of p53 or loss of p16 could be used as poor prognostic markers.