I 
from the parental, untransduced line in generating tumors. This 
study suggests that conflicting results may be obtained based on 
clone-to-clone variation in in vivo growth and tumorigenic 
capacity, suggesting that other modifications of these cells, 
caused by transfection or the subcloning procedure, affected 
their tumorgenicity. These types of clonal differences would 
likely be minimized by transducing a population of cells directly 
in vivo . 
Because the H-2K class I MHC antigen is strongly expressed 
on most tissues and can mediate an allogeneic rejection response, 
we chose it in our animal model studies designed to enhance the 
immunogenicity of tumors in vivo . These studies extend previous 
efforts to modify tumor cells by developing a system for the 
direct introduction of genes into tumors by in vivo infection 
using retroviral vectors or by DNA/liposome mediated 
transfection. This technology can also be used to deliver 
specific recombinant cytokines into the tumor microcirculation 
and to understand the immunologic basis for tumor rejection in 
vivo. 
Recombinant DNA Research, Volume 15 
[401] 
