Chromosomal translocations activating myc sequences and transduction of v-abl are critical events in the rapid induction of plasmacytomas by pristane and abelson virus

Abstract

Plasmacytomas with short latent periods can be induced in BALB/c mice by a single intraperitoneal (i.p.) injection of 0.5 ml pristane followed 20-40 d later by an injection of Abelson virus. The karyotypes of 18 such tumors were determined; 10 of these had rcpt 12;15, 5 had rcpt 6;15 and 3 had no translocations, but two of these have been shown to have interstitial deletions of chromosome 15. The specific breakpoints were the same as described in pristane-induced plasmacytomas, i.e., at 15D2 /3, 6C2 , and 12F2 . Near diploid karyotypes and trisomy of chromosome 11 were frequently seen. All of the Abelson-plus-pristane-induced plasmacytomas (ABPC) were studied as transplanted tumors, contained integrated v- abl sequences, and actively transcribed v- abl mRNA. All but one of these tumors contained abundant myc RNA transcripts. The shortness of the latent periods of the ABPC suggests that the rcpt 12;15 and rcpt 6;15 occur soon after pristane administration and are present at the time Abelson virus is introduced. In this form of plasmacytomagenesis , activated v- abl genes appear to bypass other genetic changes that require a much longer period of time in pristane plasmacytomagenesis . Nonetheless, the consistent finding of chromosome-15 alterations and abundant myc expression in these plasmacytomas emphasize the apparent need for multiple events even in the genesis of some tumors induced by rapid transforming viruses.