Trisomy of chromosome 11 (Tsll) is the second most frequent nonran dom chromosomal change in murine plasmacytomas (PCTs). The fre quency of Tsll is significantly higher in PCTs induced in pristane

Trisomy of chromosome 11 (Tsll) is the second most frequent nonran dom chromosomal change in murine plasmacytomas (PCTs). The fre quency of Tsll is significantly higher in PCTs induced in pristane conditioned mice infected by Abelson-murine leukemia virus (52%) compared to those induced by pristane alone (8J%). Although the signif icance of Tsll in mouse plasmacytomagenesis is not clearly understood it is hypothesizedthata geneor geneslocatedonchromosome(Chr)11may specifically promote the development of PCTs in which both oncogenes, c-myc and v-abl, are abundantly expressed. To test this assumption we induced PCTs by three highly effective plasmacytomagenic retroviruses: ABL-MYC, J3V1, and RIM. Nearly 90% of PCTs that arose in BALB/c, (BALB/c X DBA/2N)F1, BALBk-nulnu, and 5-month-old SCID mice infected with ABL-MYC virus were trisomic for Chr 11. In contrast, <10% of PCTs induced by J3V1 or RIM retroviral constructs encompass lag either v-myc and v-raf or c-myc and v-Ha-ms oncogenes, respectively, contained Tsll. We have also investigated whether the entire Chr 11 or any particular subregion is preferentially duplicated in the process of ABL-MYC plasmacytomagenesis. By inducing PCTs in F! heterozygous mice that are carriers of reciprocal translocations involving Chr 11 we found that the duplicated chromosomal region is located distal to the T4Dn breakpoint (11BS band) on the telomeric segment of Chr 11. The regular duplication of this chromosomal segment strongly suggests the presence of a gene or genes whose amplification is of critical importance for v-abl associated murine plasmacytomagenesis.