<綜説>発癌と免疫 (2) 化学発癌

Abstract

Creech et al. (1939) tried to induce resistance against chemical carcinogenesis by immunizing animals with a carcinogen conjugated with certain heterologous proteins and found that it was very difficult to do so. After that. Miller et al. (1947) showed that a protein fraction of the liver combined with a carcinogenic azo dye in the early stage of treatment with the dye. It is well known that this finding led him only to the "protein or enzyme-deletion theory" of carcinogenesis, but not to pay any attention to the immunological role of conjugated carcinogens. Pope et al. (1964) and others were successful in demonstrating a new antigen in viral tumors by the use of fluorescent antibodies from tumor-bearing animals. Moreover, Gold et al. (1965) elucidated antigens specific to human stomach carcinomas on geldiffusion plates by means of adsorbed antisera from heterologous animals neonatally sensitized to normal components of the human body. However, it is doubtful that these humoral antibodies play a role in inhibiting the growth of tumors. Klein et al. (1962) and others called attention to the destructive effect on tumors of lymphoid cells from the tumor-bearing animals, although the antigens and antibodies in this phenomenon have not been described. Takeda and his associates (1963, 65) showed that chemical carcinogenesis seemed to be suppressed in animals treated with a lipoprotein fraction of the tumors induced by the same carcinogen. This author's experiments investigated the possible inhibition of tumor growth by antibodies against chemically induced autochthonous tumors. An attempt was made to induce tolerance to the carcinogen by injecting newborn mice with the drug or by neonatal thymectomy. The results are open to discussion, but it may be said that specific antigens, if any, differed significantly with the nature of the tumor and with the presence or absence of malignancy. Marked effects on chemical carcinogenesis of heterologous immunizations of rats are also illustrated in the tables.