Immune Regulation of the c-myc Oncogene in a Murine B Lymphoma

Abstract

The c-myc oncogene has been implicated in a wide spectrum of B cell neoplasias (1–4) Reports of c-myc gene amplification (5), of insertion of viral elements near the c-myc promoter (1), and of point mutations within the c-myc gene (6) have appeared. However, the most frequently observed alteration is a chromosomal translocation, and usually this is to an immunoglobulin gene element (3–5). The observed amplification of the c-myc gene in some tumors led to the proposal of activation via enhanced levels of expression of c-myc RNA; however, increased transcription does not appear to be a general mechanism of activation (5). Since the first exon of the c-myc gene is often lost during translocation, it was postulated that the product of the rearranged myc gene would be different from that of the germ-line gene. However, DNA sequencing demonstrated that initiation of protein synthesis would occur within the second exon, and thus both protein products would be the same (7). Since the large majority of these modifications affect the promoter region, subtle alterations in the regulation of c-myc expression might result. Therefore we decided to examine the regulation of expression of the normal c-myc gene within a B cell system.