Mapping of the c-myc, pvt-1 and immunoglobulin kappa genes in relation to the mouse plasmacytoma-associated variant (6;15) translocation breakpoint.

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Abstract
A variant mouse plasmacytoma (MPC)‐associated translocation chromosome has arisen by pericentric inversion and exchange of the distal segments of a Robertsonian 6;15 fusion chromosome in the CAK TEPC 1198 mouse plasmacytoma, as described earlier. In situ hybridization was performed on the normal and the inverted Rb chromosomes, using myc and kappa probes. On the normal Rb chromosome, myc was in the 15 D2/3 region, whereas kappa hybridized in the 6 C2 area, as expected. On the inverted Rb chromosome, myc remains on the centrometric side of the translocation breakpoint on the chromosome 15‐derived portion, whereas kappa has moved to the chromosome 6‐derived segment that joined the same breakpoint on the telomeric side. Taken together with our recent demonstration that the murine c‐myc locus is oriented ‘head up’ on chromosome 15, and with the results of Cory and co‐workers concerning the relationship between the kappa gene and the associated pvt‐1 region in the CAK TEPC 1198 tumor, the following conclusions can be drawn: (i) in the variant translocation of the CAK TEPC 1198 MPC, the breakage occurs 3′ of the c‐myc gene, as in the human Burkitt lymphoma‐associated variant translocations; (ii) the pvt‐1 gene on chromosome 15 is distal to the myc gene; (iii) the kappa light chain locus is oriented ‘head up’ on mouse chromosome 6 and faces pvt‐1 and, beyond it, c‐myc, in a head‐to‐tail configuration.