GROWTH-INHIBITION OF HUMAN-TUMOR CELLS IN ATHYMIC MICE BY ANTI-EPIDERMAL GROWTH-FACTOR RECEPTOR MONOCLONAL-ANTIBODIES

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  • 1 January 1984
    • journal article
    • research article
    • Vol. 44  (3) , 1002-1007
Abstract
Monoclonal antibodies (MoAb) were raised against epidermal growth factor (EGF) receptors on a human epidermoid carcinoma cell line, A431. Administration of anti-EGF receptor MoAb inhibited tumor formation in athymic mice by A431 cells and by another epidermal carcinoma cell line, T222. When one of the same MoAb was used in therapy against Li-7 (a human hepatoma) and HeLa cells (a cervical carcinoma), tumor growth was not affected. The number of EGF receptors on A431 cells was about 100-fold higher than on T222, Li-7, and HeLa cells, suggesting that the number of EGF receptors may not be an important determinant in suppressing tumor growth. Three anti-EGF receptor MoAb were usedin the present studies. MoAb 528 (IgG2a) and 225 (IgG1) are capable of competing with EGF for receptor binding and inhibit proliferation of A431 cells in culture. The other MoAb, 455 (IgG1), is incapable of blocking the binding of EGF to its receptors and has no effect on the proliferation of cultured A431 cells. All 3 MoAb inhibited A431 tumor growth in athymice mice, indicating that the antibody isotype and the site of binding on the EGF receptor are not the determinants of antiproliferative activity in vivo. The observation that MoAb against the receptor for EGF is cytostatic rather than cytocidal in vitro against A431 cells, yet completely prevents tumor growth in vivo, suggests that some host animal responses also may be involved in the antitumor effect. MoAb against growth factor receptors could provide useful immunotherapeutic agents.