or mammary adenocarcinoma cells induced a potent anti-tumor 
effect mediated by infiltration of eosinophils and macrophages 
(56) . These studies demonstrate that cytokines, expressed at 
high local concentrations, are effective anti-tumor agents. 
We have previously proposed an alternative approach to 
stimulate an anti-tumor response, through the introduction of an 
allogeneic class I MHC gene into established human tumors. The 
antigenicity of tumor cells has been altered previously by the 
expression of viral antigens through infection of tumor cells 
(57-61) , or expression of allogeneic antigens introduced by 
somatic cell hybridization (62,63). Allogeneic class I MHC genes 
have been introduced into tumor cells by transfection and 
subsequent selection in vitro. These experiments have produced 
some conflicting results. In one case, transfection of an 
allogeneic class I MHC gene (H-2L^) into an H-2* 3 tumor resulted 
in immunologic rejection of the transduced cells and also 
produced transplantation resistance against the parent tumor 
cells (64) . . In another instance, transfection of H-2 melanoma 
cells with the H-2D d gene did not lead to rejection (65), however 
increased differential expression of H-2D products relative to H- 
2K may have affected the metastatic potential and immunogenicity 
of tumor cells (66) . The effects of allogeneic H-2K gene 
expression in tumor cells was examined in another study (67) . 
Several subclones which were selected in vitro and expressed an 
allogeneic gene were rejected in mice syngeneic for the parental 
tumor line, however, other subclones did not differ from the 
parental, untransduced line in generating tumors. This finding 
Recombinant DNA Research, Volume 17 
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