mice were injected with /9-galactosidase (d,X) or H-2K S (■ , • ) 
vector I plasmids. 
Mice were preimmunized by intraperitoneal injection with 10 6 
irradiated CT26 H-2K S cells 7-14 days prior to tumor inoculation. 
Injections were performed at the indicated times following tumor 
inoculation, and tumor diameter measured in two perpendicular 
dimensions using calipers. 
VIII. Efficacy of RSV expression vectors in the MCA 106 tumor 
model . 
To determine whether the RSV expression vectors were 
successful in the treatment of MCA 106 cells in vivo, an RSV K s 
plasmid with an SV40 polyadenylation sequence or an RSV K s 
plasmid with a /3-globin polyadenylation sequence, as described in 
Section 2.B.a of the "Points to Consider," were introduced into 
subcutaneous tumors as described above. Significant reduction in 
tumor growth was also observed. Of note, the survival was 
prolonged in the H-2K S treated group. Four of eight animals in 
the ^-galactosidase group expired by day 20 in this experiment, 
in contrast to 0 of 8 injected with the j9-globin or 1 of 8 in the 
RSV SV40 expression vectors. By day 25, 7 of 8 mice with /9- 
galactosidase tumors had expired, in contrast to 2 of 8 mice with 
tumors injected with H-2K S . These results indicate that 
expression vectors lacking retroviral elements are successful in 
inducing tumor regression by introduction of a foreign MHC gene. 
In this experiment, the ^-galactosidase control was an RSV £- 
galactosidase expression vector utilizing the SV40 T antigen 
polyadenylation signal. 
Recombinant DNA Research, Volume 15 
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