Abstract
In genetically susceptible BALB/cAn mice intraperitoneal injection of pristane induces plasmacytomas. More than 95% of these plasmacytomas show chromosome (6; 15) or (12;15) translocations, which result in continuous expression of c-myc (Ohno et al.1984). Direct evidence for a causative role of myc in tumor induction came from experiments using the J series of recombinant retroviruses (Rapp et al. 1985, Potter et al. 1987). The J2 and J3 viruses carry an avian MH2/MC29 hybrid v-myc and a mouse v-raf oncogene. However, in the J3 virus gag-raf gene is taken out of frame by a 256 bp deletion spanning the gag/raf border. The removal of v-raf specific sequences by this deletion leaves the minimal transforming sequence of v-raf intact (Heidecker et al., in preparation). The J5 virus carries a v-myc oncogene derived from MC29. Injection of pristane-primed mice with the J2 virus induced myeloid tumors and lymphocytic neoplasms, whereas only myeloid tumors were seen in animals inoculated with the J5 virus. Importantly, plasmacytoma development was accelerated upon infection with J3 virus.
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