A novel genetic parameter of B-CLL is the mutation status of the VH genes (123-125). Although in the past, B-CLL was considered to be a lymphoma derived from pregerminal center B-cells, somatically mutated VH genes could be demonstrated in about half of the cases in these studies. Accordingly, a separation was made into two different B-CLL groups: one with unmutated VH genes, assumed to originate in pregerminal center cells, and another with mutated VH genes, thought to stem from postgerminal center cells. Moreover, it could be demonstrated that the VH mutation status is clinically relevant. Although B-CLL with unmutated VH shows an unfavorable course, with rapid disease progression, B-CLL with mutated VH often shows slow progression
(7,8). In addition, there was a correlation between VH mutation status and CD38 expression of B-CLL cells as further evidence of the biological difference between the two forms (7). The relationship of the VH mutation status to genomic aberrations and the differential influence of these factors in the pathogenesis and progression of B-CLL are currently undergoing intensive examination.
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