The immunogenicity of recombinant canarypox (ALVAC) viral vectors within mu
rine whole-cell tumor vaccines was evaluated using the T cell thymic lympho
ma STF10 and the B16 melanoma. Tumor cells were modified with the recombina
nt ALVAC vectors and injected into syngeneic mice. Control mice receiving c
ells alone all developed tumors, while mice injected with tumor variants be
aring parental and recombinant vectors either completely rejected their tum
ors, or exhibited a significant delay in tumor formation. Rechallenge of mi
ce receiving STF10-variant vaccines yielded a protective effect against par
ental tumor cells only when a modified regimen incorporating two vaccinatio
ns was utilized. Notably, the parental ALVAC virus was equivalent to all ot
her recombinant ALVAC viruses in conferring antitumor immunity when using a
prime-and-boost protocol. Tumorigenicity experiments in nude mice revealed
that the effector mechanism mediating rejection of tumor cells bearing ALV
AC vectors is multifactorial, in that the immunogenicity of STF10/ALVAC vac
cines is reduced, but not completely abolished in these mice. Finally, in v
itro experiments revealed that cytotoxic T cells specific for parental STF1
0 cells could be generated as a result of in vivo immunization with STF10/A
LVAC vaccines.