Radon-induced cancer: a cell-based model of tumorigenesis due to protracted exposures.
Radon-induced cancer: a cell-based model of tumorigenesis due to protracted exposures.
复制标题
氡诱发的癌症：由于长期暴露而导致的基于细胞的肿瘤发生模型。
DOI：
10.1080/09553009414551771
复制
发表时间：
1994
影响因子：
2.6
通讯作者：
Elkind,MM
中科院分区：
文献类型：
--
作者：
Elkind,MM
In 1982, results with C3H mouse embryo cells showed that the frequency of neoplastic transformation was enhanced when exposures to fission-spectrum neutrons were protracted in time. This finding was unexpected because the opposite was found with low-LET radiations. Similar neutron enhancements were reported with normal life-span Syrian hamster embryo cells, and with human hybrid cells. Because other studies did not confirm the preceding, in 1990–at a conference convened by the US Armed Forces Radiobiological Research Institute—a biophysical model was proposed to explain the basis for the enhancement observed in some experiments but not in others. The model attributed special sensitivities, related to killing and neoplastic transformation, to cells in and around mitosis. Subsequently, it was shown that late G2/M phase cells constituted this window of sensitivity. In the instance of tumorigenesis, the model predicted that protracted exposures to a high-LET radiation would result in enhanced frequencies of transformation providing that susceptible cells were cycling or could be induced to cycle. The model explained data on lung tumour induction in rats breathing radon at different concentrations, and uranium miners working in atmospheres containing different concentrations of radon. The model also explains the anomalous finding that lung cancer deaths are often sublinearly correlated with indoor radon concentration.
