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.
Americas ; Asia ; Comparative Genomic Hybridization* ; Europe ; Genes, Tumor Suppressor ; Genotype* ; Herpesvirus 4, Human* ; Humans ; Killer Cells, Natural ; Lymphoma* ; Polymerase Chain Reaction ; Proto-Oncogenes