Host resistance against methylcholanthrene (MC)-induced sarcomas, demonstrated by previous authors after transplantation to isologous recipients, could also be shown to occur in the primary autochthonous host, whose tumor had been operatively removed. The autochthonous mice, together with groups of isologous animals, were pretreated with irradiated sarcoma cells and subsequently challenged with increasing doses of viable cells, also inoculated into untreated isologous controls. An increased resistance could be demonstrated with twelve out of sixteen tumors in the autochthonous and nineteen out of 22 tumors in the isologous host. Resistance was relative rather than absolute and broke down when the dose of viable cells was progressively increased. It was usually stronger in isologous than in autochthonous mice, but this was not a general rule. Isologous mice pretreated with irradiated normal tissues and subsequently challenged with viable sarcoma cells showed either no increase in resistance or a slight increase that exceeded the control level but did not reach the level found in isologous hosts pretreated with irradiated cells of the same sarcoma. Isologous, untreated mice that had received total-body irradiation before being challenged with viable sarcoma cells supported the growth of small viable inocula better than did unirradiated isologous hosts.

In the cases tested, resistance against a given sarcoma did not lead to cross-resistance against a different sarcoma, induced in the same genotype by MC. Serial treatment with homologous, MC-induced sarcoma tissue did not reduce the yield of primary sarcomas obtained after application of MC.

Lymph node cells, but not serum, of isologous mice pretreated with heavily irradiated sarcoma cells, could neutralize the sarcoma cells wholly or partially upon incubation in vitro. Lymph node cells of untreated animals and preimmunized lymph node cells killed by freezing and thawing had no effect.

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This work has been supported by grants from the National Cancer Institute, U.S. Public Health Service, and by grants from the Swedish Cancer Society and Lotten Bohmans Fund. Our thanks are due to Miss Maj-Lis Eriksson and Miss Birgitta Pettersson for valuable technical assistance.

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