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Low incidence of mbr bcl ‐2/J H fusion genes in Hodgkin's disease
Author(s) -
Kneba Michael,
Eick Stefan,
Herbst Hermann,
Pott Christiane,
Bolz Ingrid,
Dallenbach Friederike,
Hiddemann Wolfgang,
Stein Harald
Publication year - 1995
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711750404
Subject(s) - breakpoint , gene , microbiology and biotechnology , fusion gene , biology , polymerase chain reaction , reed–sternberg cell , lymph node , chromosomal translocation , immunohistochemistry , biopsy , pathology , lymphoma , genetics , medicine , immunology , hodgkin lymphoma
Lymph node biopsies from 140 cases of Hodgkin's disease (HD) and from 30 non‐malignant lesions were screened for the presence of t(14;18) translocations involving the major breakpoint region (mbr) of the bcl ‐2 gene and the joining region (J) H of the immunoglobulin heavy chain gene, using a polymerase chain reaction (PCR) assay with subsequent nucleotide sequencing of amplified bcl ‐2/J H junctional regions. Expression of the bcl‐2 protein within the Hodgkin and Reed‐Sternberg (HRS) cells was investigated in 86 cases of HD by immunohistochemistry on cryostat or paraffin sections. Although bcl ‐2 expression could be found in a proportion of neoplastic cells in up to one‐third of HD cases, the frequency of t(14;18) gene fusions detected by PCR was low. We identified such gene fusions in only 3 out of 140 (2 per cent) HD cases, one biopsy of which presented with four clonally distinct bcl ‐2/J H sequences. No t(14;18) was found in any of 30 reactive lymph node lesions. All fusion gene sequences were unique regarding the localization of the chromosome 14 and 18 breakpoints and the extranucleotide N‐insertions. None of these gene fusions conformed to t(14;18) breakpoint sequences previously characterized in our laboratories. Our findings point to a mere coincidence in some cases of HD lesions and cells carrying a t(14;18) in the same biopsy and argue against a significant role of bcl ‐2 in the pathogenesis of HD.