Evidence from proviral tagging experiments has suggested that pim-2 is
similar in oncogenic behavior to its well characterized relative pim-
1. While expression in tissues differs, both genes expressed in mitoge
nically stimulated hematopoietic cells and their transcription is indu
ced in response to the same cytokines, Expression of a pim-2 transgene
in lymphoid cells predisposed mice to T-cell lymphomas like those pro
moted by pim-1 transgenes, Moreover, strong collaboration with an E mu
-myc transgene was manifested as pre-B cell leukemia in neonate bi-tra
nsgenic animals, Remarkably, this collaboration was attenuated but not
prevented by X-inactivation of one of the transgenes. The addition of
pim-2 to the fold increases the prominence of the pim proto-oncogene
family in tumorigenesis.