Idle J R
Department of Pharmacological Sciences, Medical School, Newcastle upon Tyne, Great Britain.
Mutat Res. 1991 Apr;247(2):259-66. doi: 10.1016/0027-5107(91)90021-f.
It is now clear that tobacco smoking, alcohol consumption, dietary factors and occupation can all interact with genetic host factors to place one individual at a greater or lesser risk of a particular cancer than another. Phenotypes which confer significantly elevated risks arise from the human CYP1A1. CYP2D6, GST1 and NAT (N-acetyltransferase) genes. The last is the only one remaining to be cloned. It is envisaged that several of these genes may interact in a given circumstance cooperatively to increase susceptibility. For example CYP1A1, CYP2D6 and GST1 genotypes may have additive or multiplicative risks of bronchogenic carcinoma in cigarette smokers. CYP2D6 and NAT genotypes may interact in bladder cancer. The advent of molecular genetics brings us closer to the day when, for example, factory workers in potentially hazardous environments might be screened using PCR methodology on skin scrapings or buccal swabs for their innate susceptibility to combined workplace and lifestyle cancer risks.
现在已经明确，吸烟、饮酒、饮食因素和职业都可能与遗传宿主因素相互作用，使一个人患特定癌症的风险相对于另一个人有高有低。人类CYP1A1、CYP2D6、GST1和NAT（N - 乙酰转移酶）基因会产生显著增加风险的表型。最后一个基因是唯一尚未克隆的。可以设想，其中几个基因在特定情况下可能协同作用以增加易感性。例如，CYP1A1、CYP2D6和GST1基因型在吸烟者中可能对支气管癌有累加或倍增风险。CYP2D6和NAT基因型可能在膀胱癌中相互作用。分子遗传学的出现使我们更接近这样一天，例如，在潜在危险环境中的工厂工人可能会使用PCR方法对皮肤刮屑或口腔拭子进行筛查，以检测他们对工作场所和生活方式综合致癌风险的先天易感性。
