bcl-2 expression in Hodgkin's disease. Correlation with the t(14;18) translocation and Epstein-Barr virus

In a prior study from our laboratory using the polymerase chain reaction (PCR) technique, the t(14;18)(q32;q21) translocation was detected in low copy number in 32% of Hodgkin's disease cases. The cell of origin of the t(14;18), however, was not determined. To further investigate the role of bcl-2 in Hodgkin's disease and the possibility that the translocation resides in Reed-Sternberg and Hodgkin's (RS-H) cells, we analyzed selected cases of Hodgkin's disease immunohistologically using a monoclonal antibody reactive with bcl-2. Because Epstein-Barr virus (EBV) has been reported to upregulate bcl-2 expression, we also used an in situ method for detecting EBV in these tissues. Thirteen cases of Hodgkin's disease were studied, including seven cases with the t(14;18) translocation and six cases without it, as determined by PCR in a prior study. bcl-2 protein was detected immunohistologically in the RS-H cells in eight cases: three with the t(14;18) translocation and five in which the translocation was not detected. EBV RNA was detected in the RS-H cells of four patients, including two in which the RS-H cells also were bcl-2 positive. The presence of bcl-2 staining of the RS-H cells in this series of cases did not correlate with clinical features, histologic subtype, the presence of the t(14;18) translocation, or EBV-positivity. The lack of consistent bcl-2 protein expression in RS-H cells, including EBV-positive RS-H cells, may suggest that the t(14;18) translocation does not reside in RS-H cells in at least a subset of cases of Hodgkin's disease. If this is true, the t(14;18) translocation may not play an important role in the pathogenesis of Hodgkin's disease.