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Immunostimulation of chemical oncogenesis in the mouse
Author(s) -
Prehn Richmond T.
Publication year - 1977
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910200615
Subject(s) - spleen , carcinogenesis , immune system , immunogenicity , in vivo , stimulus (psychology) , sarcoma , biology , latency stage , neoplasm , cancer research , immunology , phenotype , pathology , medicine , cancer , genetics , psychology , gene , psychotherapist
Abstract Past work has demonstrated, both in vivo and in vitro , that a weak immune reaction can stimulate rather than inhibit the growth of many transplantable tumors. It was therefore predicted that animals with a weak immunological capacity would be more susceptible to tumor induction than would those with either a minimal or a maximal capacity. X‐rayed, thymectomized mice were inoculated with various numbers of normal syngeneic spleen cells and were subsequently exposed to various degrees of oncogenic stimulus by 3‐methylchol‐anthrene in the form of subcutaneous wafers. As expected, it was found that among animals exposed to a high oncogenic stimulus, the sarcoma incidence was significantly higher among those animals that had received small numbers (10 4 ) of spleen cells than among those that had either received none (0) or the maximal number (10 7 ). In contrast, when the oncogenic stimulus was low, the tumor incidence was the same in all groups regardless of the numbers of spleen cells the animals had received. Since the average immunogenicity of sarcomas has been shown to be directly related to the concentration of the chemical oncogen and inversely to the tumor latency, it can be inferred that the higher tumor incidence associated with 10 4 spleen cells in the experiments with a high oncogenic stimulus probably depended upon the immunogenicities of the induced tumors and was therefore consistent with an immunostimulation of oncogenesis.