Mutation Of The Cd79b Gene

lowing cross-linking of surface immunoglobulin, and a functional BCR is essential for B-cell development and the survival of peripheral B cells.

Patients with CLL have reduced or absent expression of the extracellular domain of CD79B. Two groups of investigators have identified mutations in a subset of CLL cases in either exon 4 or 5 of the CD79B gene, which encode the transmembrane and cytoplasmic domains of CD79B protein, respectively.47,48 Transfection of mutant CD79B genes into Jurket T cells resulted in either a failure of CD79B cells surface expression or impaired signal transduction.49 The pattern of CD79B mutations in CLL is similar to that seen in immunoglobulin V genes, and it has been suggested that CD79B mutations arise through somatic hypermutation. However, these results remain controversial, and other data have suggested that CD79B mutations are polymorphisms and that alternative splicing of the CD79B gene can result in loss of exon 3, which encodes the extracellular domain.50 Alternatively spliced variants may be found in normal as well as in malignant B cells, and it remains to be seen whether CD79B mutations are transforming events in CLL or whether loss of surface membrane CD79B expression is a secondary phenomenon, possibly arising because CLL cells no longer require a functional BCR for cell survival.

The B-cell antigen receptor (BCR) comprises surface immunoglobulin and heterodimers of two accessory proteins, CD79A and CD79B. The BCR mediates signal transduction fol-

Table 6-4. BCL2 Rearrangements in Chronic Lymphocytic

Leukemia

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