Exploration and analysis of differentially expressed genes in EpsteinBarr virus negative and positive plasmablastic lymphoma
Clin. transl. oncol. (Print)
; 25(10): 2884-2891, oct. 2023. ilus
Article
in English
| IBECS
| ID: ibc-225069
Responsible library:
ES1.1
Localization: ES15.1 - BNCS
ABSTRACT
Objectives Plasmablastic lymphoma (PBL) is a subtype of diffuse large B-cell lymphoma (DLBCL) often associated with EpsteinBarr virus (EBV) infection. Despite recent advances in treatment, PBL still has a poor prognosis. EBV is listed as one of the human tumor viruses that may cause cancer, and is closely related to the occurrence of some nasopharyngeal carcinoma (NPC), lymphoma and 10% of gastric cancer (GC). It is very important to explore the differentially expressed genes (DEGs) between EBV-positive and EBV-negative PBL. Through bioinformatics analysis of DEGs between EBV-positive PBL and EBV-negative PBL, we gain a deeper understanding of the pathogenesis of EBV-positive PBL. Methods We selected the GSE102203 data set, and screened the DEGs between EBV-positive PBL and EBV-negative PBL. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were applied. The proteinprotein interaction (PPI) network was constructed, and screened for the hub genes. Finally, Gene Set Enrichment Analysis (GSEA) was performed. Results In EBV-positive PBL, the immune-related pathway is upregulated and Cluster of differentiation 27 (CD27) and programmed cell death-ligand 1 (PD-L1) are hub genes. Conclusions In EBV-positive PBL, EBV may affect tumorigenesis through activation of immune-related pathways and upregulation of CD27, PD-L1. Immune checkpoint blockers of CD70/CD27 and programmed cell death 1 (PD-1)/PD-L1 pathways may be one of the effective strategies for the treatment of EBV-positive PBL (AU)
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Collection:
National databases
/
Spain
Database:
IBECS
Main subject:
Lymphoma, Large B-Cell, Diffuse
/
Epstein-Barr Virus Infections
/
Plasmablastic Lymphoma
Limits:
Humans
Language:
English
Journal:
Clin. transl. oncol. (Print)
Year:
2023
Document type:
Article
Institution/Affiliation country:
Qingdao University/China