Ehrlich
tumor expresses the
ganglioside GT1b. The plasma of mice with
Ehrlich ascites tumor burden also contains GT1b. The structural identity of plasma GT1b was ascertained by a series of enzymatic degradation and mass spectral analysis. Mice were vaccinated with purified plasma GT1b admixed with
Freund's adjuvant (FA). Sixty nine percent suppression of
Ehrlich ascites tumor growth was observed in vaccinated mice. The suppression was dose-dependent. It is hypothesized that the
tumor growth-suppression is a result of immune response to GT1b Humoral immune response to GT1b was demonstrated by passive hemagglutination assay of the sera of vaccinated mice. To test the hypothesis, the mice were administered with rabbit polyclonal anti-GT1b
IgM antibody in varying doses and challenged with Ehrlich
tumor. A significant reduction in
tumor growth (65%) was observed in mice administered with anti-GT1b
IgM antibody. Again, the suppression was dose-dependent. To verify further, another batch of mice was immunized with
anti-idiotypic antibodies to rabbit anti-GT1b
IgM raised in rat. The polyclonal anti-idiotype antibody is expected to carry the structural image of GT1b. In a dose-dependent manner, a maximum of 82% suppression of
tumor growth was observed in mice immunized with the anti-idiotype antibody. This observation further strengthened the hypothesis that
ganglioside mediated suppression of
tumor growth may be a result of immunogenicity of the target
ganglioside. This was also supported by positive reaction of the sera of anti-idiotype vaccinated mice with both anti-idiotype antibody and
ganglioside GT1b in passive hemagglutination assay. The results favour the therapeutic potential of immunogenic
tumor-associated
gangliosides.