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Apoptosis‐related genes and proteins in Hodgkin's disease
Author(s) -
Lauritzen Anne F.,
Møller Peter Horn,
Nedergaard Trine,
Guldberg Per,
HouJensen Klaus,
Ralfkiaer Elisabeth
Publication year - 1999
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1999.tb01453.x
Subject(s) - phenotype , null cell , apoptosis , reed–sternberg cell , biology , gene , microbiology and biotechnology , genotype , programmed cell death , epstein–barr virus , pathogenesis , cancer research , lymphoma , immunology , pathology , virus , genetics , medicine , hodgkin lymphoma
During recent years it has become increasingly evident that L&H cells in nodular lymphocytic predominance (LP) Hodgkin's disease (HD) and Hodgkin and Reed‐Sternberg (H‐RS) cells in approximately half the cases of classical HD originate from B‐lymphocytes, and that H‐RS cells in most of the remaining cases of classical HD express a null phenotype. The pathogenesis of HD is unknown. An association with Epstein‐Barr virus (EBV) has been suggested and there are also indications that genes involved in programmed cell death (apoptosis) may be implicated. In this study, the expression of four apoptosis‐related proteins (bcl‐2, bcl‐x, bax and p53) in 53 cases of HD was examined and the data were correlated with the genotype, the EBV status and the phenotype (B, T or null) of the neoplastic cells. The H‐RS cells expressed a B‐cell phenotype in 3/3 cases of nodular LP and in 19/50 (38%) cases of classical HD. The remaining cases showed a null‐cell phenotype in 29/50 (58%) and a T‐cell phenotype in 2/50 (4%). EBV was more often positive in B (14/19, 74%) than in null (7/29, 24%) type HD. The H‐RS cells were bcl‐2‐positive in 19/53 (36%), bcl‐x‐positive in 17/53 (32%), bax‐positive in 1/53, and p53‐positive in 41/53 (77%) cases. No relationship was found between bcl‐2 expression and EBV status, or between bcl‐2 and bcl‐x expression. A t(14;18) translocation was seen in 2 of 34 cases. P53 point mutations were not detected. Our findings indicate that nodular LP and classical HD originate from B‐cells in a high proportion of cases. They also suggest a role for bcl‐2, bcl‐x and p53 in tumorigenesis. The pathogenesis is not known at this stage.