[Bases on timing of combined modality of chemotherapy and immunotherapy].
Chemoimmunotherapy with anticancer drugs and immunoregulatory drugs and cytokines is a logical combination of 2 forms of therapy that have different mechanisms of action and no overlapping toxicity. Generally, anticancer drugs show rapidly the strong suppressive effect on tumor growth but also on host hemato-immunological functions. On the other hand, immunotherapy demonstrate the potential of restoring the hemato-immunological dysfunction of chemotherapy as well as the gradual antitumor effect through activating host defense mechanisms against cancer, indicating that these therapeutic modalities are complementary. On these biological rationale of chemoimmunotherapy mentioned above, we have demonstrated that immunostimulant, Nocardia-CWS is capable of producing tumoricidal macrophages being different from anticancer drugs in cytotoxic mechanism against cancer, and also that macrophage tumoricidal activity is significantly suppressed by exposure to anticancer drug, mitomycin C. Another beneficial activity of immunostimulant showed in our previous studies is a capability of production of colony stimulating activities. In a cooperative study with lung cancer patients it has been shown that recovery of leucopenia after chemotherapy is accelerated by administration of immunostimulant, MDP-Lys. Recently, immunomodulatory lymphokine, IL-2, has been clinically used for induction of activated killer lymphocytes (LAK cells) with tumoricidal activity. According to our studies, however, anticancer drug, when administered to cancer patients or added directly to culture of lymphocytes with IL-2 for LAK induction, shows significant suppressive effect on LAK induction. Considering these experimental and clinical studies, it can be concluded that immunotherapy, when employed as adjuvant after chemotherapy, play the important roles not only in eradication of tumor cells being escaped from chemotherapy but also in prevention of infections complication by activating host defense mechanisms common to cancer and infection.
Third Dept. of Internal Medicine, School of Medicine, Tokushima University.
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D000970:Antineoplastic Agents / Q000627:therapeutic use*; D003131:Combined Modality Therapy; D006801:Humans; D007116:Immunization, Passive; D007155:Immunologic Factors / Q000627:therapeutic use*; D007372:Interferons / Q000627:therapeutic use; D007376:Interleukin-2 / Q000627:therapeutic use; D015979:Killer Cells, Lymphokine-Activated / Q000637:transplantation; D009369:Neoplasms / Q000188:drug therapy / Q000276:immunology / Q000628:therapy*; D013997:Time Factors
D000970:Antineoplastic Agents; D007155:Immunologic Factors; D007376:Interleukin-2; D007372:Interferons