c-mycHypermutation in Burkitt's Lymphoma

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Abstract
Translocation between the c-myc protooncogene and one of the three immunoglobulin loci is a cytogenetic hallmark of the B cell tumor, Burkitt's lymphoma. The resulting deregulation of c-myc expression is a critical step in tumorigenesis. The translocation breakpoint may lie within c-myc proper, in which case deregulation is due, in part, to dissociation of key 5′ regulatory sequences from the protein-coding portions of the gene. Alternatively, the breakpoint may flank c-myc, leaving the gene grossly intact. In these latter cases, mutation, which may be extensive, is usually seen within c-myc, specifically at or near the same key regulatory sequences. The precise contribution of these mutations to c-myc deregulation is gradually being clarified. The mechanisms underlying c-myc mutations are not known. Hypermutation in c-myc may reflect the influence of the juxtaposed immunoglobulin gene, which is subject to hypermutation during an intermediate stage of normal B lymphoid development. This relationship, however, has not been firmly established.