Bouchardy C, Benhamou S, Dayer P
Geneva Cancer Registry, Switzerland.
Cancer Res. 1996 Jan 15;56(2):251-3.
The genetically determined P450 CYP2D6 activity is suspected to be involved in lung carcinogenesis by activating carcinogens contained in tobacco smoke. Therefore, lung cancer risk should depend on both smoking exposure and CYP2D6 activity. The extent to which CYP2D6 activity, determined by using dextromethorphan, could modify the effect of tobacco was evaluated from a study on 128 lung cancers and 157 controls. A strong interaction was observed; the effect of tobacco on lung cancer risk rose with increasing CYP2D6 activity (P < 0.001). Increasing levels of smoking increased lung cancer risk only among smokers with the highest CYP2D6 activity, and CYP2D6 was a risk factor only among heavy smokers. Smokers with both the highest CYP2D6 activity and daily tobacco consumption were at very high risk for lung cancer. These results may explain discrepant results of previous studies on the association between CYP2D6 activity and lung cancer.
基因决定的细胞色素P450 CYP2D6活性被怀疑通过激活烟草烟雾中的致癌物而参与肺癌的发生。因此，肺癌风险应取决于吸烟暴露量和CYP2D6活性。通过使用右美沙芬测定的CYP2D6活性对烟草影响的改变程度，在一项针对128例肺癌患者和157例对照的研究中进行了评估。观察到一种强烈的相互作用；烟草对肺癌风险的影响随着CYP2D6活性的增加而上升（P < 0.001）。吸烟量增加仅在CYP2D6活性最高的吸烟者中增加肺癌风险，且CYP2D6仅在重度吸烟者中是一个风险因素。CYP2D6活性最高且每日吸烟量最大的吸烟者患肺癌的风险非常高。这些结果可能解释了先前关于CYP2D6活性与肺癌关联的研究结果不一致的情况。
