enhancement of pim-1 expression with the greatest frequency and enhancement 
occurring when the virus is inserted within the 3' -terminal exon (Selten et 
al.. 1986). Pim-1 is most homologous to the protein-serine kinases and is 
presumably a lymphoid-specific protein kinase involved with lymphocyte 
proliferation (Selten et al.. 1986). Studies of the murine T cell lymphoma 
line LSTRA reveal enhanced expression of a lymphocyte-specific protein kinase 
(Voronova et al.. 1984; Maith et al.. 1985) by promoter insertion of the tck 
gene which is also a T cell specific protein kinase. The tck gene is not 
identical to the pim-1 gene nor is it identical to the mis-l/pvt-1 gene 
(Veronova and Sefton. 1986) which is associated with B cell lymphomas In mice 
and T cell lymphoma in rats. While the majority of T cell lymphomas In newborn 
mice appear to occur near the pim-1 gene, insertion in thymic lymphomas has 
been described near c-myc (Cuypers et al., 1984; Corconvan et al.. 1984; 
Seltan, 1984). In rats Moloney MuLV causes thymic lymphomas when inserted In 
three loci Mlvi-1. Mlvi-2. and Mlvi-3 in addition to c-myc (Ts i chi is. 1985). 
Mlvi-2 may also be involved in murine T cell lymphomas (Tsichlis. 1984). 
The literature shows that the majority of murine T cell lymphomas induced 
by Moloney MuLV result in increased expression of a protein kinase produced by 
a gene located within the pim-1 locus. Other proto-oncogenes have been 
described that result in malignant transformation, yet some lymphomas remain to 
be explained. The most common method by which lymphomas are induced appears to 
be insertion within the 3' -terminal exon; however, insertion outside of the 
gene and promoter insertion are also mechanisms. 
Another consideration in the potential for malignant tranformation is 
viral tropism. Slowly transforming retroviruses appear to have some tissue 
specificity in the cells they transform, and subsequently the type of tumor 
they produce. The main determinant of malignant potential for many 
[58] Recombinant DNA Research, Volume 12 
