Epstein-Barr virus (EBV) has a pathogenic role in several lymphomas, including diffuse large B-cell lymphoma (DLBCL). EBV-associated genetic aberrations in DLBCL have not been fully characterized. The aim of this study was to investigate the prevalence of EBV infection in sporadic DLBCL cases in Kuwait and to evaluate their EBV status in relation to demographic data, the anatomical disease site, immunophenotypic features, particularly pertaining to the Choi's DLBCL prognostic classification, and chromosomal aberrations. Using immunohistochemistry (IHC), in situ hybridization (ISH), nested polymerase chain reaction (nPCR) and comparative genomic hybridization techniques, formalin-fixed paraffin-embedded blocks of archived DLBCL cases were included and evaluated in the study. EBV was detected in 6.9, 18.2 and 25% of the studied cases using IHC, ISH and nPCR, respectively, indicating that nPCR is more sensitive in detecting EBV than IHC and ISH. EBV- DLBCL cases showed BCL6 protein expression more frequently than EBV+ DLBCL cases. The reported prevalence of EBV+ DLBCL cases in this study is similar to that reported in the literature using ISH results and higher using nPCR results. There was a significant inverse correlation between BCL6 protein expression and the presence of EBV (p = 0.01).
Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous group of diseases that have diverse clinical, pathological, and biological features. Here, it is shown that primary nodal and extranodal DLBCLs differ genomically and phenotypically. Using conventional comparative genomic hybridization (CGH), the authors assessed the chromosomal aberrations in 18 nodal, 13 extranodal, and 5 mixed DLBCLs. The results demonstrate significantly distinct chromosomal aberrations exemplified by gains of chromosomal arms 1p, 7p, 12q24.21-12q24.31, and 22q and chromosome X and loss of chromosome 4, 6q, and 18q22.3-23 in extranodal compared with nodal DLBCLs. Nodal DLBCLs showed an increased tendency for 18q amplification and BCL2 protein overexpression compared with extranodal and mixed tumors. Using a panel of five antibodies against GCET1, MUM1, CD10, BCL6, and FOXP1 proteins to subclassify DLBCLs according to the recent Choi algorithm, the authors showed that the genomic profiles observed between the nodal and extranodal DLBCLs were not due to the different proportions of GCB vs ABC in the two groups. Further delineation of these genomic differences was illuminated by the use of high-resolution 21K BAC array CGH performed on 12 independent new cases of extranodal DLBCL. The authors demonstrated for the first time a novel genome and proteome-based signatures that may differentiate the two lymphoma types.
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