Abstract: Provided is a method for enhancing the efficacy of cancer vaccines, such as tumor vaccines. The method involves administering to an individual who is in need of therapy for a tumor an anti-cancer agent and an agent that causes depletion of myeloid cells and/or inhibits recruitment of myeloid cells to the tumor. The effect of the anti-cancer agent on the tumor is greater relative to the effect of the anti-cancer agent in the absence of the anti-myeloid cell agent. Also provided is a method for identifying candidates for the therapy. This approach involves determining if an individual has a tumor characterized by undesirable myeloid cell proliferation and/or tumor infiltration and/or myeloid cell recruitment to the tumor, and if such determination is made, designating the individual as a candidate for the therapy. In one embodiment, the identification of the individual as such a candidate is followed by the therapeutic approach.

Abstract: Mutant ras oncogene peptides may induce specific anti-ras cellular immune responses in vaccinated patients. Moreover, a human CD8+ CTL epitope(s) reflecting a specific point mutation in the K-ras oncogene at codon 12 was identified. The mutant ras peptide has implications for both active and passive immunotherapies in selected carcinoma patients. A nested 10-mer peptide was identified [i.e., ras5-14(Asp12)], which was shown to bind to HLA-A2 and display specific functional capacity for expansion of the in vivo-primed CD8+ CTL precursors.

Abstract: Mutant ras oncogene peptides may induce specific anti-ras cellular immune responses in vaccinated patients. Moreover, a human CD8+ CTL epitope(s) reflecting a specific point mutation in the K-ras oncogene at codon 12 was identified. The mutant ras peptide has implications for both active and passive immunotherapies in selected carcinoma patients. A nested 10-mer peptide was identified [i.e., ras5-14(Asp12)], which was shown to bind to HLA-A2 and display specific functional capacity for expansion of the in-vivo-primed CD8+ CTL precursors.

Abstract: Mutant ras oncogene peptides may induce specific anti-ras cellular immune responses in vaccinated patients. Moreover, a human CD8+ CTL epitope(s) reflecting a specific point mutation in the K-ras oncogene at codon 12 was identified. The mutant ras peptide has implications for both active and passive immunotherapies in selected carcinoma patients. A nested 10-mer peptide was identified [i.e., ras5-14(Asp12)], which was shown to bind to HLA-A2 and display specific functional capacity for expansion of the in vivo-primed CD8+ CTL precursors.