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Epstein–Barr virus ( EBV )‐positive diffuse large B‐cell lymphoma ( DLBCL ) of the elderly ( EBV [+] DLBCL ‐E) is classified as a subtype of  DLBCL . Until now, its molecular pathogenesis has remained unknown. To identify pathways characteristic of  EBV (+) DLBCL ‐E, gene expression profiling of five  EBV (+) DLBCL ‐E and seven  EBV ‐negative  DLBCL  ( EBV [−] DLBCL ) cases was undertaken using human oligonucleotide microarray analysis. Gene set enrichment analysis and gene ontology analysis showed that gene sets of the Janus kinase‐signal transducer and activator of transcription ( JAK ‐ STAT ) and nuclear factor kappa B ( NF ‐κB) pathways were enriched in  EBV (+) DLBCL ‐E cases. To confirm the results of the expression profiles,  in vitro  analysis was performed. Expression profiling analysis showed that high activation of the  JAK ‐ STAT  and  NF ‐κB pathways was induced by  EBV  infection into  DLBCL  cell lines. Activation of the  NF ‐κB pathway was confirmed in  EBV ‐infected cell lines using an electrophoretic mobility shift assay. Western blot analysis revealed an increased protein expression level of phosphorylated signal transducer and activator of transcription 3 ( STAT 3) in an  EBV ‐infected cell line. Protein expression of phosphorylated  STAT3  was frequently observed in lymphoma cells of  EBV (+) DLBCL ‐E clinical samples using immunohistochemistry ( EBV [+] DLBCL ‐E: 80.0% [ n  = 20/25] versus  EBV [−] DLBCL : 38.9% [ n  = 14/36];  P  =   0.001). The results of the present study suggest that activation of the  JAK ‐ STAT  and  NF ‐κB pathways was characteristic of  EBV (+) DLBCL ‐E, which may reflect the nature of  EBV ‐positive tumor cells. Targeting these pathways as therapies might improve clinical outcomes of  EBV (+) DLBCL ‐E.

cancer science

Gene expression profiling of Epstein–Barr virus‐positive diffuse large B‐cell lymphoma of the elderly reveals alterations of characteristic oncogenetic pathways