Background: Expression of STK40 is observed in some cancer types, while its role in lowgrade gliomas (LGG) is unclear. The present study aimed to demonstrate the relationship between STK40 and LGG based on The Cancer Genome Atlas (TCGA) database and bioinformatics analysis. Methods: Kruskal-Wallis test, Wilcoxon sign-rank test, and logistic regression were used to evaluate the relationship between clinicopathological features and STK40 expression. Kaplan-Meier method and Cox regression analysis were used to evaluate prognostic factors. Gene set enrichment analysis (GSEA) and immuno-infiltration analysis were used to determine the significant involvement of STK40 in function. Results: High STK40 expression in LGG was associated with WHO grade (P<0.001), IDH status (P<0.001), primary therapy outcome (P=0.027), 1p/19q codeletion (P<0.001) and histological type (P<0.001). High STK40 expression predicted a poorer overall survival (OS) (HR: 3.07; 95% CI: 2.09-4.51; P<0.001), progression-free survival (PFS) (HR:2.11; 95% CI: 1.59-2.81; P<0.001) and disease specific survival (DSS) (HR: 3.27; 95% CI: 2.17-4.92; P<0.001). STK40 expression (HR: 2.284; 95% CI: 1.125-4.637; P=0.022) was independently correlated with OS in LGG patients. GSEA demonstrated that pathways including cell cycle mitotic, neutrophil degranulation, signaling by Rho GTPases, signaling by interleukins, M phase, PI3K-Akt signaling pathway and naba secreted factors were differentially enriched in STK40 high expression phenotype. Immune infiltration analysis showed that STK40 expression was correlated with some types of immune infiltrating cells. Conclusion: STK40 expression was significantly correlated with poor survival and immune infiltration in LGG, and it may be a promising prognostic biomarker in LGG.

Background Approximately 60% of patients with autoimmune encephalitis (AE) exhibit secondary acute symptomatic seizures and showed highly sensitive to immunotherapy. However, it is difficult for many patients to receive early immunotherapy since the early identification of the cause in AE is more complex. This study aimed to investigate the early predictors of initial immune-related seizures and to guide the evaluation of treatment and prognosis. Methods One hundred and fifty-four patients with new-onset “unknown etiology” seizures with a course of disease less than 6 months were included. Serum and/or cerebrospinal fluid neuron-specific autoantibodies (NSAbs), including N-methyl-D-aspartate receptor (NMDAR), α-amino-3-hydroxy-5- Methyl-4-isoxazole propionic acid receptor 1 (AMPAR1), AMPAR2, anti-leucine rich glioma inactivated 1 antibody (LGI1), anti-gamma-aminobutyric acid type B receptor (GABABR), anti-contact protein-related protein-2 (CASPR2) were used to screen for immune etiology of the seizures. In addition, patients with epilepsy and encephalopathy were also examined via brain MRI, long-term video EEG, antibody prevalence in epilepsy and encephalopathy (APE2) score, and modified Rankin Scale (mRS). A logistic regression model was used to analyze the early predictors of immune etiology. Results Thirty-four cases (22.1%) were positive for NSAbs. Among all 154 patients, 23 cases of autoimmune encephalitis (AE) (21 cases of NSAbs positive), 1 case of ganglionic glioma (NSAbs positive), 130 cases of epilepsy or seizures (12 cases of NSAbs positive) were recorded. Also, there were 17 patients (11.0%) with APE2 ≥ 4 points, and all of them met the clinical diagnosis of AE. The sensitivity and specificity of APE2 ≥ 4 points for predicting AE were 73.9% and 100%. The results of multivariate analysis showed that the NSAbs and APE2 scores independently influenced the early prediction of initial immune-related seizures (P < 0.05). Conclusion NSAbs and APE2 scores could act as early predictors of initial immune-related seizures.

Background: Approximately 60% of patients with autoimmune encephalitis (AE) exhibit secondary acute symptomatic seizures and showed highly sensitive to immunotherapy. However, it is difficult for many patients to receive early immunotherapy since the early identification of the cause in AE is more complex. This study aimed to investigate the early predictors of initial immune-related seizures and to guide the evaluation of treatment and prognosis. Methods:One hundred and fifty-four patients with new-onset "unknown etiology" seizures with a course of disease less than 6 months were included. Serum and/or cerebrospinal fluid neuron-specific autoantibodies (NSAbs), including N-methyl-D-aspartate receptor (NMDAR), α-amino-3-hydroxy-5- Methyl-4-isoxazole propionic acid receptor 1 (AMPAR1), AMPAR2, anti-leucine rich glioma inactivated 1 antibody (LGI1), anti-gamma-aminobutyric acid type B receptor (GABABR), anti-contact protein-related protein-2 (CASPR2) were used to screen for immune etiology of the seizures. In addition, patients with epilepsy and encephalopathy were also examined via brain MRI, long-term video EEG, antibody prevalence in epilepsy and encephalopathy (APE2) score, and modified Rankin Scale (mRS). A logistic regression model was used to analyze the early predictors of immune etiology. Results: Among all patients, 34 cases (22.1%) were positive for NSAbs. Of these 34, 23 cases of autoimmune encephalitis (AE) (21 cases of NSAbs positive), 2 cases of viral encephalitis, 1 case of ganglionic glioma (NSAbs positive), 128 cases of epilepsy or seizures (12 cases of NSAbs positive) were recorded. Also, there were 19 patients (12.3%) with APE2 ≥ 4 points and 17 patients (89.5%) in the AE group. The sensitivity and specificity of APE2 ≥ 4 points for predicting AE were 73.9% and 98.5%. The results of multivariate analysis showed that the NSAbs and APE2 scores independently influenced the early prediction of initial immune-related seizures (P < 0.05). Conclusions: NSAbs and APE2 scores could act as early predictors of initial immune-related seizures.