Walker C, Goldsworthy T L, Wolf D C, Everitt J
Chemical Industry Institute of Toxicology, Research Triangle Park, NC 27709.
Science. 1992 Mar 27;255(5052):1693-5. doi: 10.1126/science.1553556.
A single germ line gene mutation at a tumor susceptibility locus in a rodent model of hereditary human renal cancer caused a 70-fold increase in susceptibility to chemical carcinogenesis. A carcinogen that targeted both renal epithelial and mesenchymal cells caused an increase in tumors of epithelial origin in susceptible animals; the number of carcinogen-induced mesenchymal tumors was unaffected by the presence of the mutation at the susceptibility locus. Thus, this mutation defines a genetic locus for susceptibility to carcinogen-induced tumors and modulation of carcinogen susceptibility by this locus exhibits cell-type specificity.
在遗传性人类肾癌啮齿动物模型中,肿瘤易感性位点的单个种系基因突变导致对化学致癌作用的易感性增加了70倍。一种靶向肾上皮细胞和间充质细胞的致癌物,在易感动物中导致上皮来源肿瘤的增加;致癌物诱导的间充质肿瘤数量不受易感性位点突变的影响。因此,这种突变定义了一个对致癌物诱导肿瘤的易感性基因位点,并且该位点对致癌物易感性的调节表现出细胞类型特异性。