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Institute for Genetics, Department of Immunology [M. M., R. K., K. R.], and the Department for Internal Medicine I [M. M., D. R., J. W., V. D., R. K.], University of Cologne, 50931 Köln, and Department of Pathology [A. B., M-L. H.], University of Frankfurt, 60596 Frankfurt, Germany
Hodgkin and Reed-Sternberg (H/RS) cells in classical Hodgkin’s disease
(cHD) are thought to be derived from preapoptotic germinal center B
cells. However, little is known about the transforming events rescuing
the precursor of the H/RS cells from apoptosis. Given the importance of
CD95 (Apo-1/Fas)-mediated apoptosis for negative selection within the
germinal center, single micromanipulated H/RS cells from 10 cases of
cHD were analyzed for somatic mutations within the CD95
gene. Three clonal mutations within the 5' regions were amplified from
single H/RS cells in one case. From H/RS cells of another case, two
mutations within the last exon coding for the death domain were
detected. About half of these H/RS cells carried a monoallelic
stop-codon; the remaining tumor cells harbored a monoallelic
replacement mutation. Both mutations likely impair CD95
function. Because all these H/RS cells also bear clonal mutations
inactivating the I
B
gene, the
IB mutations occurred earlier than
those of the CD95 gene in the sequence of transforming
events leading to cHD. In conclusion, somatic mutations of the
CD95 gene occur in a fraction of cHD cases and may favor
the escape of the precursor of the H/RS clone from apoptosis.
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