The role of host immunity in the response to chemotherapy of a mouse mammary adenocarcinoma (T1699) was investigated. Suppression of the host response by previous irradiation or ALS (antilymphocyte serum) treatment considerably decreased the therapeutic effect of both cyclophosphamide and melphalan. The timing of drug administration to normal tumor‐bearing mice was critical as the response depended on the development of an anti‐tumor immune response by the host and not solely on the size of the tumor. Although the majority of tumor‐bearing mice with demonstrable anti‐tumor immunity showed complete tumor regression when treated with cyclophosphamide or melphalan, animals that failed to respond to melphalan initially, as well as responder animals whose tumor recurred, did not respond to a second dose of drug. Neither melphalan nor cyclophosphamide suppressed the ability of the host effector cells found within the tumor mass to kill target tumor cells in the colony inhibition assay.
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Radov et al. (1976) studied this question.
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