Objectives. Glioma patients with brain tumor-related epilepsy (BTRE) have a complex profile due to the simultaneous presence of two pathologies, glioma and epilepsy; however, they have not traditionally received as much attention as those with more malignant brain tumors. The underlying pathophysiology of brain tumor-related epilepsy remains poorly understood. The purpose of this study was to investigate the possible correlation between molecular neuropathology and glioma with BTRE and a wide range of BTRE-associated molecular markers of glioma patients. Methods. A retrospective cohort study of 186 glioma patients was evaluated at our hospital, of which 64 had BTRE. The chi-square test, Spearman rank correlation, and multivariate logistic analyses were used to identify clinicopathological factors associated with BTRE in glioma patients. Results. Of the 186 patients examined in this study, 64 (34.4%) had BTRE. Based on the analysis of the characteristics of these patients, the results showed that patient age (over 40 years; P = 0.007 ), low WHO grade (grade I, II; P = 0.001 ), IDH-1 positive mutation ( P = 0.027 ), low ATR-X expression level ( OR = 0.44 ; 95% CI: 0.21, 0.92), and low Ki-67 PI ( OR = 0.25 ; 95% CI: 0.10, 0.68) were associated with the occurrence of BTRE. In our cohort, BTRE patients did not differ by sex, tumor location, or expression of olig-2 and CD34. The results of the matching study showed that low Ki-67 PI and negative ATR-X expression levels were independent factors for a higher incidence of preoperative seizures in glioma patients. Conclusion. The current study updates existing information on genetic markers in gliomas with BTRE and explores the correlation of a wide range of clinicopathological factors and glioma patients with BTRE and suggests three putative biomarkers for BTRE: positive IDH1 mutation, low Ki-67 PI, and negative ATR-X expression. These factors may provide insights for developing a more thorough understanding of the pathogenesis of epilepsy and effective treatment strategies aimed at seizure control.

Objective. Research over the past decade has suggested important roles for pseudogenes in gliomas. Our previous study found that the RPL4P4 pseudogene is highly expressed in gliomas. However, its biological function in gliomas remains unclear. Methods. In this study, we analyzed clinical data on patients with glioma obtained from The Cancer Genome Atlas (TCGA), the Chinese Glioma Genome Atlas (CGGA), the Genotype-Tissue Expression (GTEx), and the GEPIA2 databases. We used the R language for the main analysis. Correlations among RPL4P4 expression, pathological characteristics, clinical outcome, and biological function were evaluated. In addition, the correlations of RPL4P4 expression with immune cell infiltration and glioma progression were analyzed. Finally, wound healing, Transwell, and CCK-8 assays were performed to analyze the function of RPL4P4 in glioma cells. Result. We found that RPL4P4 is highly expressed in glioma tissues and is associated with poor prognosis, IDH1 wild type, codeletion of 1p19q, and age. Multivariate analysis and the nomogram model showed that high RPL4P4 expression was an independent risk factor for glioma prognosis and had better prognostic prediction power. Moreover, high RPL4P4 expression correlated with immune cell infiltration, which showed a significant positive association with M2-type macrophages. Finally, RPL4P4 knockdown in glioma cell lines caused decreased glioma cell proliferation, invasion, and migration capacity. Conclusion. Our data suggest that RPL4P4 can function as an independent prognostic predictor of glioma. It also shows that RPL4P4 expression correlates with immune cell infiltration and that targeting RPL4P4 may be a new strategy for the treatment of glioma patients.