Antiapoptotic marker, Bcl-X-L, expression on Reed-Sternberg cells of Hodgkin's disease using a novel monoclonal marker, YTH-2H12

Inhibitors of apoptosis may regulate tissue differentiation and promote cell survival in neoplasia. A new apoptosis inhibitor of the bcl-2 gene family, bcl-X-L, was recently found in some types human neoplasia but not in normal tissue. We investigated bcl-X-L expression in 419 cases of normal and neoplastic lymphoid lesions using immunohistochemistry with the monoclonal antibody bcl-X-L (YTH-2H12). Ninety-four percent (141/150) of classic Hodgkin's disease (HD) were positive for bcl-X-L with strong intensity in most Reed-Sternberg (RS) cells. Forty-eight percent (38/80) of nodular lymphocyte predominance (LPHD) were positive. In the non-Hodgkin's lymphomas (NHL), bcl-X-L was expressed in a low percentage of cases (<20%), with the exception of follicle center lymphoma, grade III/III (78%). All reactive hyperplastic lesions were negative for bcl-X-L. RS cells, which expressed bcl-X-L, were not labeled by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). We found RS cells expressing bcl-X-L were absent of DNA fragmentation (apoptosis). Our data provide evidence that bcl-XL is abnormally expressed in the RS cells of HD and some types of NHL raising speculation that inhibition of apoptosis may be important in the pathogenesis of lymphoma, specifically HD. In addition, the previously reported correlation between bcl-X-L and Epstein-Barr virus expression in HD was not supported by this study. HUM PATHOL 30:1065-1070. Copyright (C) 1999 by W.B. Saunders Company.