Garte S, Zocchetti C, Taioli E
Nelson Institute of Environmental Medicine, New York University Medical Center, NY, USA.
IARC Sci Publ. 1997(142):251-64.
Metabolic susceptibility genes are important determinants of individual susceptibility to the effects of environmental carcinogens. These genes follow the form of 'type 2' gene-environment interaction, whereby the polymorphic genetic risk factor functions only in the presence of an environmental exposure. Two different effects of carcinogen dose have been observed for these genes. Sometimes, increasing dose leads to a decreasing interaction, so that cases with the genetic risk factor have lower exposures than those cases without it. Other examples of a direct dose effect, whereby increasing exposure leads to increased interaction, have also been described. We propose a model based on multiple logistic regression to assess the nature of the dose effect in this type of gene-environment interaction. This model allows for distinction between these two dose effects, and other effects such as protective or non-interactive effects of environmental and genetic risk factors.
代谢易感性基因是个体对环境致癌物影响易感性的重要决定因素。这些基因遵循“2型”基因-环境相互作用的形式，即多态性遗传风险因素仅在存在环境暴露时起作用。对于这些基因，已观察到致癌物剂量的两种不同效应。有时，剂量增加会导致相互作用减弱，因此携带遗传风险因素的病例比不携带该因素的病例暴露水平更低。也有其他直接剂量效应的例子，即暴露增加会导致相互作用增强。我们提出了一个基于多元逻辑回归的模型，以评估这种类型的基因-环境相互作用中剂量效应的性质。该模型能够区分这两种剂量效应以及其他效应，如环境和遗传风险因素的保护或非交互效应。
