Background Recent studies have revealed that the splicing factor neuro-oncological ventral antigen 1 (NOVA1) is enriched in fibroblasts and accumulated T cells of tertiary lymphoid structures. In the present study, we investigated NOVA1 expression in various subtypes of mature and immature T- and natural killer (NK)-cell lymphomas as well as in various B-cell lymphoma subtypes. Methods: NOVA1 immunoexpression was evaluated in hyperplastic palatine tonsils (n = 20), T- and NK-cell lymphomas (n = 177), diffuse large B-cell lymphomas (n = 151), and other types of B cell lymphomas (n = 31). Nuclear staining intensity and percentage of positive tumor cells were graded. NOVA1 mRNA expression was analyzed in various lymphoma cell lines. Results: Tumor cells of T- and NK-cell lymphomas showed higher expression levels of NOVA1 than did normal paracortical T cells, and 56.5% of T- and NK-cell lymphoma cases showed diffuse and strong expression. The NOVA1 expression level varied according to the subtype; it was higher in angioimmunoblastic T-cell lymphoma, anaplastic lymphoma kinase (ALK)-negative anaplastic large cell lymphoma (ALCL), and T lymphoblastic leukemia/lymphoma (T-LBL), but it was lower in ALK-positive ALCL. In almost all B-cell lymphomas, NOVA1 expression was very low or negative. NOVA1 mRNA was also expressed in Jurkat, a T-LBL cell line. Conclusions: The present findings suggest that NOVA1 upregulation may be involved in certain subtypes of T- and NK-cell lymphomas, but not in B-cell lymphomas. Upregulated NOVA1 expression seems to be a specific biological feature of activated T cells such as T- and NK-cell lymphomas.
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NK/T cell lymphoma is a distinct clinicopathologic entity which is more prevalent in Asia than in America and Europe and is highly associated with Epstein-Barr virus (EBV) infection. Although the clinicopathologic features of the tumor have been clearly defined, genetic changes and roles of virus associated with the development and progression of tumor have not been well studied. In this study, we carried out polymerase chain reaction (PCR) for EBNA-3B, EBNA-3C, and LMP-1 30 bp deletion to investigate EBV subtype and variants in tumor tissue and performed comparative genomic hybridization (CGH) to screen chromosomal imbalances using frozen tissues from 7 patients with nasal-type NK/T cell lymphoma and 1 patient with blastic NK cell lymphoma. Of 6 cases infected with EBV, there were EBV type 1 in six, LMP-1 30 bp deletion variant in four, and LMP-1 40 bp deletion variant in one. Frequent chromosomal imbalances included deletions at 1p31-pter (4), 12q23-q24 (3), and 17p (4), and gains at 2q (5), 10q (3), and 13q34-qter (4). Blastic NK cell lymphoma displayed deletions of 9q, 7q, and 6q, similar to that of nasal-type NK/T-cell lymphoma. With these results, we assumed that candidate genes in these imbalanced chromosomal loci would provide the clue for further molecular studies to identify putative tumor suppressor genes or proto-oncogenes associated with pathogenesis of this neoplasm.