Sequence of the murine and human cellular myc oncogenes and two modes of myc transcription resulting from chromosome translocation in B lymphoid tumours.

Open Access
Publisher Website
Google Scholar
Abstract
The 15;12 chromosome translocation in murine plasmacytomas and the 8;14 in human Burkitt lymphomas often link the cellular myc oncogene to the locus for constant regions of immunoglobulin heavy chains (CH locus). To clarify how and why c‐myc translocation occurs, we have sequenced the mouse and human c‐myc genes and correlated c‐myc transcription with c‐myc rearrangement. Both genes comprise three exons; the second and third encode the myc polypeptide, which is conserved between mammals and birds, particularly in its more basic C‐terminal half. Southern blots showed that four of 12 Burkitt lines have c‐myc linked near CH switch regions and two near the joining region (JH) locus. Hence, immunoglobulin recombination machinery may participate in translocation, although the common myc breakpoint region around exon 1 does not resemble a switch region. Tumours with breakpoints just 5′ to exon 1, or distant from c‐myc, had normal c‐myc mRNAs of 2.25 and 2.4 kb, which differ at their 5′ ends, while tumours with breakpoints within exon 1 or intron 1 had altered c‐myc mRNAs (2.1‐2.7 kb in Burkitt lines), initiated within intron 1. Both types of mRNAs probably yield the same polypeptide. Since the untranslocated c‐myc allele was generally silent, translocation to the CH locus must induce constitutive c‐myc expression. The presence of c‐myc mRNA in immortal but non‐tumorigenic lymphoblastoid cell lines may implicate c‐myc in an immortalization step.