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Purpose: Glioma is the most common primary tumor in the brain, accounting for 81% of intracranial malignancies. Nowadays, cancer immunotherapy has become a novel and revolutionary treatment for patients with advanced, highly aggressive tumors. However, to date, there are no effective biomarkers to reflect the response of glioma patients to immunotherapy. In this study, we aimed to assess the clinical predictive value of ITGB2 in patients with glioma. Methods: The correlation between ITGB2 expression levels and glioma progression was explored and validated using data from CGGA, TCGA, GEO datasets, and patient samples from our hospital. Univariate and multivariate cox regression models were developed to determine the predictive role of ITGB2 on the prognosis of patients with glioma. The relationship between ITGB2 and immune activation was then analyzed. Finally, we predicted the immunotherapy response in both high and low ITGB2 expression subgroups. Results: ITGB2 was significantly elevated in gliomas with higher malignancy and predicted poor prognosis. In multivariate analysis, the hazard ratio for ITGB2 expression (low versus high) was 0.71 with 95% CI (0.59–0.85) (P < 0.001). Furthermore, we found that ITGB2 stratified glioma patients into high and low ITGB2 expression subgroups, exhibiting different clinical outcomes and immune activation status. At last, we demonstrated that glioma patients with high ITGB2 expression levels had better immunotherapy response. Conclusions: This study demonstrated ITGB2 as a novel predictor for clinical prognosis and response to immunotherapy in gliomas. Assessing expression levels of ITGB2 is a promising method to discover patients that may benefit from immunotherapy. [ABSTRACT FROM AUTHOR]

To the best of our knowledge, this is the largest clinical retrospective study in AN‐SAH patients, and is the first time to establish accurate predictive models paired with bleeding pattern. Background: Angiogram‐negative subarachnoid hemorrhage (AN‐SAH) has a definite incidence of delayed cerebral ischemia (DCI) and poor clinical outcomes. The purpose is to screen independent factors and establish a nomogram to guide the clinical therapy and assess post‐discharge prognosis. Methods: We identified 273 consecutive patients referred to our institute from 2013 to 2018 for AN‐SAH. A nomogram to predict poor outcomes was formulated based on the multivariable models of independent risk factors. The accuracy and discrimination of nomograms were determined in training and internal validation cohorts. Results: The overall poor outcome rates of AN‐SAH were 14.3% and 8.7% at 3 months and 12 months, respectively. In addition, perimesencephalic AN‐SAH (PAN‐SAH) presented with a more unfavorable prognosis compared with non‐perimesencephalic AN‐SAH (NPAN‐SAH). The clinical prognosis was associated with the World Federation of Neurosurgical Societies scale (WFNS) (odds ratio, 3.82 [95% CI, 1.15‐12.67] for 3‐month outcome; and odds ratio, 31.69 [95% CI, 3.65‐275.43] for 12‐month outcome), Subarachnoid hemorrhage Early Brain Edema Score (SEBES) (odds ratio, 10.39 [95% CI, 1.98‐54.64] for 3‐month outcome; odds ratio, 10.01 [95% CI, 1.87‐53.73] for 12‐month outcome), and symptomatic vasospasm (odds ratio, 3.16 [95% CI, 1.03‐9.70] for 3‐month outcome; odds ratio, 5.15 [95% CI, 1.34‐19.85] for 12‐month outcome). The nomogram was constructed based on the above features, which represented great predictive value in clinical outcomes. Conclusions: Symptomatic vasospasm, high WFNS, cerebral edema, and NPAN‐SAH after hemorrhage were associated with poor outcome of AN‐SAH. The nomogram with WFNS (3‐5), SEBES (3‐4), vasospasm, and NPAN‐SAH represented a practical approach to provide individualized risk assessment for AN‐SAH patients. [ABSTRACT FROM AUTHOR]

Aim: To demonstrate the clinical value of epithelial membrane protein 3 (EMP3) with bioinformatic analysis and clinical data, and then to establish a practical nomogram predictive model with bicenter validation. Methods: The data from CGGA and TCGA database were used to analyze the expression of EMP3 and its correlation with clinical prognosis. Then, we analyzed EMP3 expression in samples from 179 glioma patients from 2013 to 2017. Univariate and multivariate cox regression were used to predict the prognosis with multiple factors. Finally, a nomogram to predict poor outcomes was formulated. The accuracy and discrimination of nomograms were determined with ROC curve and calibration curve in training and validation cohorts. Results: EMP3 was significantly higher in higher‐grade glioma and predicted poor prognosis. In multivariate analysis, high expression of EMP3 (HR = 2.842, 95% CI 1.984–4.071), WHO grade (HR = 1.991, 95% CI 1.235–3.212), and IDH1 mutant (HR = 0.503, 95% CI 0.344–0.737) were included. The nomogram was constructed based on the above features, which represented great predictive value in clinical outcomes. Conclusion: This study demonstrated EMP3 as a novel predictor for clinical progression and clinical outcomes in glioma. Moreover, the nomogram with EMP3 expression represented a practical approach to provide individualized risk assessment for glioma patients. [ABSTRACT FROM AUTHOR]