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High- (Cl-33H) and low- (Cl-35L) metastatic clones were established from a methylcholanthrene-induced rat fibrosarcoma (FMQ-100). The modal chromosome numbers of the two clones were different. These clones grew in in vitro culture, showing similar growth rate and saturation density. However, in in vivo experiments, Cl-33H exhibited a higher tumor growth rate, tumorigenicity, spontaneous metastatic potential, and experimental metastatic potential than did Cl-35L. Alveolar macrophages obtained from normal syngeneic rats stimulated growth of these clones in vitro, as assessed by [3H]thymidine uptake. Moreover, this effect was greater on Cl-33H than Cl-35L. The growth-promoting effect of macrophages was also observed under the in vitro condition of lack of direct contact between macrophages and tumor cells. These results suggested the possibility that alveolar macrophage-derived growth-promoting factors play some role in the development of pulmonary metastasis in this tumor system, and the difference of susceptibility to the growth-promoting factors might be one of the causes of the different metastatic potentials of Cl-33H and Cl-35L.
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