Abstract
The concept that tumor-specific immune responses may effectively control or even suppress tumor growth has developed from studies showing that immunity can be induced against many, although by no means all, experimentally induced animal tumors when transplanted into syngeneic hosts (Hellström and Hellström, 1969b; Sjögren, 1965; Baldwin, 1973). This was originally established in tests with animal tumors, either induced by chemical carcinogens or oncogenic viruses, or arising spontaneously, showing that syngeneic hosts preimmunized against tumor, e.g., by implantation of radiation-attenuated tumor cells, rejected a subsequent challenge graft of the same tumor. Following this, it was found in a number of instances that animals with a transplanted tumor developing at one site and which is beyond host control can, nevertheless, reject a concomitant challenge with the same tumor implanted at another site, providing that the challenge inoculum is not too great (Gershon et al., 1967; Vaage, 1971; Deckers et al., 1973; Chandradasa, 1973). This indicates that the tumor-bearing host has developed an effective immune response to tumor implanted at a second site and implies that either the response was too weak or developed too slowly to cause rejection of the primary tumor implant, or that, alternatively, host factor(s) may have modified the initial tumor-immune response.
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Baldwin, R.W., Robins, R.A. (1975). Humoral Factors Abrogating Cell-Mediated Immunity in the Tumor-Bearing Host. In: Arber, W., et al. Current Topics in Microbiology and Immunology. Current Topics in Microbiology and Immunology, vol 72. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66289-8_2
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