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Experimental Therapeutics |
College of Biological Sciences, Department of Microbiology [N. K. D., P. T. P. K.], College of Medicine, Obstetrics and Gynecology [D. B. D., V. C. S., P. T. P. K.], Internal Medicine [P. L. T.], and Medical Biochemistry [P. T. P. K.], and the Comprehensive Cancer Center [P. L. T., V. C. S., P. T. P. K.], The Ohio State University, Columbus, Ohio 43210
Synthetic peptide vaccines targeting B-cell epitopes of the extracellular domain of the HER-2 oncoprotein were evaluated for their capacity to elicit HER-2-specific antibodies with antiproliferative activity. Several HER-2 B-cell epitopes were identified by computer-aided analysis of protein antigenicity, and selected B-cell epitopes were synthesized colinearly with a promiscuous T-helper epitope (208–302) derived from the measles virus fusion protein at either the NH2 or COOH terminus linked via a four-residue turn sequence (GPSL). In addition, one epitope sequence, 628–647, was mutated to optimize disulfide pairing to mimic the native HER-2 receptor. All of the four selected epitopes elicited high-titered antibodies in outbred rabbits with exceptionally high titers for MVF-HER-2(628–647). These antibodies were cross-reactive with the native HER-2 receptor. Antibodies elicited by MVF HER-2(628–647) inhibited proliferation of human HER-2-overexpressing breast cancer cells in vitro and caused their antibody-dependent cell-mediated cytotoxicity. Furthermore, immunization with MVF-HER-2(628–647) prevented the spontaneous development of HER-2/neu-overexpressing mammary tumors in 83% of transgenic mice. The engineered, chimeric peptide B-cell immunogen MVF-HER-2(628–647) may have applications in the prevention of HER-2-overexpressing cancers.
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