| Abstract: | The frequent trisomy of murine chromosome 15 in T lymphomas suggests that it bears one or more genes conducive to T-cell neoplasia. One such gene seems to be c-myc, the oncogene frequently activated in B-lymphoid tumours either by retroviral insertion, as in the avian bursal lymphomas, or by a translocation to the immunoglobulin heavy-chain locus, as in the predominant t(12; 15) of murine plasmacytomas and the analogous t(14; 8) of human Burkitt lymphomas. The c-myc gene was strongly implicated in T-cell neoplasia when 15-25% of T lymphomas arising in AKR mice, a strain prone to leukaemia, were found to have retroviral inserts near c-myc. Proviruses near c-myc were also found in several T lymphomas induced by murine leukaemia viruses (MuLV) in both mice and rats, but many of the rat thymomas bear an insert instead at one of several other common sites, at least two of which have murine homologues on chromosome 15. We show here that some murine T lymphomas contain proviral inserts in the recently identified chromosome 15 locus for plasmacytoma variant (6; 15) translocations, which we have denoted pvt-1. Although 6; 15 breakpoints map cytogenetically to the same chromosome band as c-myc, the alterations of pvt-1 in tumours occur at least 72 kilobases (kb) from the c-myc promoters. The insertions in T lymphomas suggest that an altered pvt-1 locus is conducive to neoplasia in T cells as well as B cells, possibly via long-range effects on c-myc expression. |
