DNA sequences involved in the rearrangement and expression of the murine c-myc gene.

Abstract

The characteristic chromosomal translocation found in many B cell tumors results in the joining of a c-myc oncogene (from murine chromosome 15) to an immunoglobulin heavy chain switch region (chromosome 12—Perry, 1983; Robertson, 1983). This translocation has several consequences. One is that the c-myc gene is frequently truncated, losing part or all of its 5′-most exon (Stanton et al., 1983; ar-Rushdi, et al., 1983; Gelman, et al., 1983; Saito, et al., 1983). A second is increased transcription of the truncated c-myc gene; this transcription often originates from adventitious promotors in the first intron (Stanton, et al., 1983; Hamlyn and Rabbitts, 1983; Mushinski et al., 1983; Adams et al., 1983; Erikson, et al., 1983a). Many have hypothesized that a third consequence of this rearrangement is oncogenesis. In virtually all chicken lymphomas induced by avian leukosis virus, the c-myc gene has been activated by proviral insertion (Hayward, et al., 1981). On the other hand, in erythroblastoid tumors induced by the same virus, c-myc is never activated (however, c-erb is activated—Fung, et al., 1983). The conclusion from chickens, that activation of c-myc is necessary for lymphomagenesis, would also seem to apply to activation of murine c-myc by translocation.