The Activity of an ABL-MYC Retrovirus in Fibroblast Cell Lines and in Lymphocytes

Abstract

Evidence from many laboratories indicates that v-abl and c-myc oncogenes both can participate in the induction of B-cell neoplasia, and under appropriate conditions both may synergize in that process. The first indication of the interaction of these two oncogenes was the experiments of Potter et al (1973) in which it was found that infection of pristane-primed mice with Abelson murine leukemia virus (A-MuLV) greatly decreased the latent period for plasmacytoma development. Molecular analysis of those tumors indicated that most tumors expressed the v-abl oncogene product and contained a c-myc gene deregulated by chromosomal translocation (Ohno et al 1984) . Although c-myc deregulation has clearly been implicated in plasmacytoma development (Shen-Ong et al 1982; Adams et al 1983; Mushinski et al 1983), retroviruses that express v-myc or c-myc appear to induce tumors of the myeloid series of cells (Bambaugh et al 1985; Vennstrom et al 1984) . Moreover, infection with A-MuLV does not accelerate plasmacytoma development in Eμ-myc transgenic mice (Dyall-Smith et al 1988) . On the other hand, spleen cells from such mice can develop into plasmacytomas following infection with A-MuLV (Sugiyama et al 1989) . To investigate the interaction of v- abl and c-myc deregulated oncogenes under conditions where both are introduced simultaneously into cells we have constructed a virus that expresses both genes.