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*
Surgery Branch, National Cancer Institute,
Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, and
Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD 20892
Tumor Ag-specific vaccines used for cancer immunotherapy can
generate specific CD8 responses detectable in PBMCs and in
tumor-infiltrating lymphocytes. However, human studies have shown that
detection of a systemic vaccine-induced response does not necessarily
correlate with the occasional instances of tumor rejection. Because
this discrepancy might partially be attributable to the genetic
heterogeneity of human cancers, as well as to the immunosuppressive
effects of previous treatments, we turned to a mouse model in which
these variables could be controlled to determine whether a relationship
exists between the strength of vaccine-induced immune responses and
tumor rejection. We challenged mice with the 
-galactosidase
(-gal)-expressing tumor cells, C25.F6, vaccinated them with
-gal-carrying viral vectors, and used quantitative RT-PCR to measure
the vaccine-induced immune response of splenocytes directly ex vivo. We
found that the strength of the response increased with increasing doses
of -gal-carrying vector and/or upon boosting with a heterologous
-gal-carrying virus. Most importantly, we found that the strength of
the detected immune response against this foreign Ag strongly
correlated with reduction in the number of lung metastases. The results
from this mouse model have major implications for the implementation of
tumor vaccines in humans.
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