Wu R L, Kearney R
Br J Cancer. 1979 Mar;39(3):241-6. doi: 10.1038/bjc.1979.47.
The mechanisms of non-specific resistance to syngeneic methylcholanthrene-induced fibrosarcomas of mice were investigated. Results showed that a small tumour graft of 0.05 X 10(5) cells is greatly enhanced in growth when admixed with large numbers of cell fragments, killed cells or viable non-replicating cells. The enhancement of small tumour grafts in cell mixtures was found to be non-specific. Carrageenan, a known anti-macrophage agent, significantly increased tumour growth in normal mice. However, it did not enhance the increased tumour growth of 0.05 X 10(5) cells mixed with 10(6) viable, non-replicating mitomycin C-treated tumour cells. The latter observation indicates that carrageenan and admixed cells interfere with the same tumour-inhibitory mechanism and therefore cannot produce additive effects. The results give support to the concept of a non-specific macrophage "surveillance" system which appears crucial in controlling tumour growth, since it determines the establishment of small numbers of tumour cells while they can still be easily destroyed.
对小鼠同基因甲基胆蒽诱导的纤维肉瘤的非特异性抗性机制进行了研究。结果表明,当与大量细胞碎片、死亡细胞或存活的非复制细胞混合时,0.05×10⁵个细胞的小肿瘤移植瘤生长显著增强。发现细胞混合物中小肿瘤移植瘤的增强是非特异性的。角叉菜胶是一种已知的抗巨噬细胞剂,可显著增加正常小鼠的肿瘤生长。然而,它并没有增强与10⁶个存活的、经丝裂霉素C处理的非复制肿瘤细胞混合的0.05×10⁵个细胞的肿瘤生长增加。后一观察结果表明,角叉菜胶和混合细胞干扰相同的肿瘤抑制机制,因此不能产生相加效应。这些结果支持了非特异性巨噬细胞“监测”系统的概念,该系统在控制肿瘤生长中似乎至关重要,因为它决定了少量肿瘤细胞在仍易于被破坏时的定植。