CELL-PROLIFERATION IN CARCINOGENESIS
CELL-PROLIFERATION IN CARCINOGENESIS
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DOI：
10.1126/science.2204108
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发表时间：
1990-08-31
期刊：
影响因子：
56.9
通讯作者：
ELLWEIN, LB
中科院分区：
文献类型：
--
作者：
COHEN, SM;ELLWEIN, LB
在动物生物测定中，高剂量诱发癌症的化学物质往往不符合遗传毒素的传统特征。这些非遗传毒性化合物（如糖精钠）中的许多化合物都具有增加靶器官中细胞增殖的共同特性。一个基于生物学的，计算机化的致癌作用的描述被用来表明，细胞增殖的增加可以解释非遗传毒性化合物的致癌性。遗传毒性化学品（如2-乙酰氨基芴）的致癌剂量-反应关系也部分归因于细胞增殖增加。要确定非遗传毒性化学品的增殖（和致癌）反应阈值的存在，并估计人类接触的风险，就需要有机理方面的信息。.
Chemicals that induce cancer at high doses in animal bioassays often fail to fit the traditional characterization of genotoxins. Many of these nogenotoxic compounds (such as sodium saccharin) have in common the property that they increase cell proliferation in the target organ. A biologically based, computerized description of carcinogenesis was used to show that the increase in cell proliferation can account for the carcinogenicity of nongenotoxic compounds. The carcinogenic dose-response relationship of genotoxic chemicals (such as 2-acetylaminofluorene) was also due in part to increased cell proliferation. Mechanistic information is required for determination of the existence of a threshold for the proliferative (and carcinogenic) response of nongenotoxic chemicals and the estimation of risk for human exposure. .