Effect of immune status on the development of artificially induced metastases in different anatomical locations.

Abstract

Summary Using a syngeneic methylcholanthrene-induced mouse sarcoma of recent origin and with demonstrated immunogenicity, we studied the effect of the immune status of the host on tumor growth in four different anatomical locations. For simulation of metastatic spread, tumor cells were selectively “seeded” in the lungs via the tail vein and in the liver via hepatic portal vein injection. Tumor growth was also studied in s.c. and i.p. injection sites. Host resistance following sensitization was expressed most strongly in the liver and lungs and less strongly in the s.c. and i.p. locations. Sensitization by living tumor implants surgically removed after a period of growth left the hosts more resistant than the mice with sensitizing implants that had been killed by local irradiation. Immunotherapy consisting of s.c. injection of killed tumor tissue after challenge in addition to presensitization resulted in stronger resistance than presensitization alone. The incidence of tumor growth was higher in sublethally irradiated mice than in untreated, normal control mice. This indicates that even the presumably weak first phase of the developing immune response initiated in control mice by the challenge implant was important in controlling the development of tumor growth.