Identifying the Hub Genes of Glioma Peritumoral Brain Edema Using Bioinformatical Methods

Abstract

Glioma peritumoral brain edema (GPTBE) is a frequent complication in patients with glioma. The severity of peritumoral edema endangers patients’ life and prognosis. However, there are still questions concerning the process of GPTBE formation and evolution. In this study, the patients were split into two groups based on edema scoring findings in the cancer imaging archive (TCIA) comprising 186 TCGA-LGG patients. Using mRNA sequencing data, differential gene (DEG) expression analysis was performed, comparing the two groups to find the key genes affecting GPTBE. A functional enrichment analysis of differentially expressed genes was performed. Then, a protein–protein interaction (PPI) network was established, and important genes were screened. Gene set variation analysis (GSVA) scores were calculated for major gene sets and comparatively correlated with immune cell infiltration. Overall survival (OS) was analyzed using the Kaplan–Meier curve. A total of 59 DEGs were found, with 10 of them appearing as important genes. DEGs were shown to be closely linked to inflammatory reactions. According to the network score, IL10 was in the middle of the network. The presence of the IL10 protein in glioma tissues was verified using the human protein atlas (HPA). Furthermore, the gene sets’ GSVA scores were favorably linked with immune infiltration, particularly, with macrophages. The high-edema group had higher GSVA scores than the low-edema group. Finally, Kaplan–Meier analysis revealed no differences in OS between the two groups, and eight genes were found to be related to prognosis, whereas two genes were not. GPTBE is linked to the expression of inflammatory genes.

Peritumoral Edema in Gliomas: A Review of Mechanisms and Management

“…However, in the presence of excess fluid, fluid pooling and subsequent edema occur. As gliomas grow, they secrete angiogenic factors such as vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs) [52][53][54][55]. These factors increase the vascular permeability of the BBB, allowing plasma to enter the extracellular space and leading to edema formation.…”

Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema

“…Additional bioinformatic analysis of ‘The Cancer Genome Atlas’ (TCGA) data revealed that occurrence of tumor-related brain edema affects inflammatory gene expression, e.g. by increasing IL-10 levels ( 12 ), which in turn was shown to promote glioma cell invasion ( 13 , 14 ). As a result, the threshold for T cell activation can be raised, and their antitumor activity can be directly suppressed ( 15 ).…”