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Blood, Vol. 94 No. 10 (November 15), 1999:
pp. 3516-3522
Analysis of the B-Cell Receptor B29 (CD79b) Gene in Familial
Chronic Lymphocytic Leukemia
Béatrice Payelle-Brogard,
Christian Magnac,
Francesca R. Mauro,
Franco Mandelli, and
Guillaume Dighiero
From the Unité d'Immunohématologie et
d'Immunopathologie, Institut Pasteur, Paris, France; and the
Dipartimento di Biotecnologie Cellulari ed Ematologia, Università
di Roma "La Sapienza", Rome, Italy.
The B-cell antigen receptor (BCR) comprises membrane Igs (mIgs) and
a heterodimer of Ig (CD79a) and Ig (CD79b) transmembrane proteins, encoded by the mb-1 and B29 genes, respectively. These accessory proteins are required for surface expression of mIg and BCR
signaling. B cells from chronic lymphocytic leukemia (B-CLL) frequently
express low to undetectable surface Ig, as well as CD79b protein.
Recent work described genetic aberrations affecting B29 expression
and/or function in B-CLL. Because the prevalence of CLL is increased
among first degree relatives, we analyzed the B29 gene in 10 families
including 2 affected members each. A few silent or replacement
mutations were observed at the genomic level, which never lead to
truncated CD79b protein. Both members of the same family did not harbor
the same mutations. However, a single silent base change in the B29
extracellular domain, corresponding to a polymorphism, was detected on
1 allele of most patients. These results indicate that the few
mutations observed in the B29 gene in these patients do not induce
structural abnormalities of the CD79b protein and thus do not account
for its low surface expression in B-CLL. Furthermore, genetic factors
were not implicated, because identical mutations were not observed
among 2 members of the same family.
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