EBV and malignant lymphoma with special emphasis on pyothorax-associated lymphoma.

Abstract

The etiologic role of Epstein-Barr virus (EBV) for B lymphomagenesis has been postulated from epidemiologic and in vitro studies. There is now a substantial body of evidence linking EBV to African Burkitt’s lymphoma, which is a B-cell lymphoma (Klein 1985). An association between EBV and human malignancies, including Hodgkin’s disease (Weiss et al. 1987) and non-Hodgkin’s lymphomas of either B- or T-cell immunophenotypes (Hochberg et al. 1983; Hamilton-Dutoit et al. 1992), has been reported. EBV-positive rate in immunocompetent patients with nodal lymphomas is less than 10% in B-cell and approximately 50% in T-cell lymphoma (Aozasa et al. 1998). The criteria for defining cases as EBV-positive includes (1) presence of EBV genome by Polymerase chain reaction (PCR), and (2) positive signals for EBV in large tumor cells by DNA or RNA in situ hybridization (ISH) using EBV-encoded small nuclear early region-1 (EBER1) probe. Among extranodal lymphomas, nasal natural killer (NK)-cell lymphoma, pyothorax-associated lymphoma (PAL), and adrenal lymphoma are EBV-associated; the EBV-positive rate is over 90% in the nasal lymphoma and PAL and approximately 50% in the adrenal lymphoma.