ArticleScientific reports2023
Bioinformatics analysis of the pathogenic link between Epstein-Barr virus infection, systemic lupus erythematosus and diffuse large B cell lymphoma.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- KIF23 in disease pathogenesis and therapeutics : from molecular mechanisms to clinical translation.Cancer cell international · 2026Review
- KIF23 in disease pathogenesis and its therapeutic and diagnostic potential.Discover oncology · 2026Review
- Controlling gene expression through five zinc finger domains of ZNF18.Protein science : a publication of the Protein Society · 2025Article
- Cancer in connective tissue disease.Frontiers in immunology · 2025Review
- Machine learning and validation reveal that immune-related genes in systemic lupus erythematosus regulate apoptosis and cycle progression in diffuse large B-cell lymphoma.Frontiers in medicine · 2025Article
- Machine learning insights into vaccine adjuvants and immune outcomes.Frontiers in immunology · 2025Article
- Roles of DEPDC1 in various types of cancer (Review).Oncology letters · 2024Review
- Article
- A multi-tissue, splicing-based joint transcriptome-wide association study identifies susceptibility genes for breast cancer.American journal of human genetics · 2024Article
- Evaluation of Genes and Molecular Pathways Common between Diffuse Large B-cell Lymphoma (DLBCL) and Systemic Lupus Erythematosus (SLE): A Systems Biology Approach.Medical journal of the Islamic Republic of Iran · 2024Article
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1 author at 1 institution in 1 country.
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Abstract
Epstein-Barr virus (EBV) is a risk factor for diffuse large B-cell lymphoma (DLBCL) and systemic lupus erythematosus (SLE). While prior research has suggested a potential correlation between SLE and DLBCL, the molecular mechanisms remain unclear. The present study aimed to explore the contribution of EBV infection to the pathogenesis of DLBCL in the individuals with SLE using bioinformatics approaches. The Gene Expression Omnibus database was used to compile the gene expression profiles of EBV-infected B cells (GSE49628), SLE (GSE61635), and DLBCL (GSE32018). Altogether, 72 shared common differentially expressed genes (DEGs) were extracted and enrichment analysis of the shared genes showed that p53 signaling pathway was a common feature of the pathophysiology. Six hub genes were selected using protein-protein interaction (PPI) network analysis, including CDK1, KIF23, NEK2, TOP2A, NEIL3 and DEPDC1, which showed preferable diagnostic values for SLE and DLBCL and involved in immune cell infiltration and immune responses regulation. Finally, TF-gene and miRNA-gene regulatory networks and 10 potential drugs molecule were predicted. Our study revealed the potential molecular mechanisms by which EBV infection contribute to the susceptibility of DLBCL in SLE patients for the first time and identified future biomarkers and therapeutic targets for SLE and DLBCL.
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