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Suppression of established pulmonary metastases by murine melanoma-specific monoclonal antibodies
V J Hearing1, S P Leong, W D Vieira
1Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
The intravenous administration of melanoma-specific monoclonal antibodies (MAbs) 9B6 and T97, both of the IgG2b isotype, consistently suppressed the growth of established JB/MS murine melanoma lung metastases. This activity was not dose-dependent, lower doses of MAbs often being more suppressive than higher doses. Intravenous administration of antibodies at days 5 and 8 following challenge appeared to be optimal for suppression whereas no inhibition was seen with intravenous treatment at days 0 and 3 or at days 10 and 13. Consistent and significant inhibition was also observed using established B16F10 lung metastases but only at lower doses, whereas both MAbs were ineffective against the T92497 sarcoma in syngeneic mice. These MAbs appear to act not as direct anti-tumor agents but as host immune response regulators, since specific anti-tumor effects were abrogated in tumor-bearing hosts following pre-treatment with antibodies directed against asialo-GM1 and NK-1.1, surface markers of natural killer cells.
The intravenous administration of melanoma-specific monoclonal antibodies (MAbs) 9B6 and T97, both of the IgG2b isotype, consistently suppressed the growth of established JB/MS murine melanoma lung metastases. This activity was not dose-dependent, lower doses of MAbs often being more suppressive than higher doses. Intravenous administration of antibodies at days 5 and 8 following challenge appeared to be optimal for suppression whereas no inhibition was seen with intravenous treatment at days 0 and 3 or at days 10 and 13. Consistent and significant inhibition was also observed using established B16F10 lung metastases but only at lower doses, whereas both MAbs were ineffective against the T92497 sarcoma in syngeneic mice. These MAbs appear to act not as direct anti-tumor agents but as host immune response regulators, since specific anti-tumor effects were abrogated in tumor-bearing hosts following pre-treatment with antibodies directed against asialo-GM1 and NK-1.1, surface markers of natural killer cells.