Risk of head and neck cancer and the alcohol dehydrogenase 3 genotype.
Risk of head and neck cancer and the alcohol dehydrogenase 3 genotype.
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头颈癌的风险和乙醇脱氢酶 3 基因型。
DOI：
10.1093/carcin/22.1.57
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发表时间：
2001
期刊：
影响因子：
4.7
通讯作者：
Bell,DA
中科院分区：
文献类型：
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作者：
Olshan,AF;Weissler,MC;Watson,MA;Bell,DA
头颈部鳞状细胞癌(SCCHN)包括口腔、咽部和喉部，是评估酒精和酒精代谢酶(如酒精脱氢酶)等基因-环境相互作用的良好肿瘤模型。我们进行了一项以医院为基础的病例对照研究，包括182例新诊断的SCCHN患者和202例需要手术的头颈部非肿瘤性疾病的对照。对终生饮酒和ADH3‘快速’等位基因(ADH3*1)的联合作用与SCCHN的风险进行了评估。在调整吸烟、年龄、性别和种族的情况下，用Logistic回归估计饮酒与ADH3基因之间的交互作用。交互作用在乘性和加性两个尺度上进行了评估。每周饮用40杯或更多酒精饮料，患SCCHN的风险增加近6倍[优势比(OR)=5.9；95%可信区间(CI)=2.0-17.7；调整了年龄、性别、种族和吸烟年限]。我们没有发现ADH3*1纯合子(OR=0.9；CI=0.4-1.9)或杂合子(OR=0.8；CI=0.4-1.7)与ADH3*2纯合子相比有任何风险增加。没有迹象表明任何酒精使用变量与ADH3*1基因之间存在交互作用。例如，包括每周平均饮酒量和ADH3基因类型在内的交互作用项无显著意义(P=0.22)。这项研究并没有指出ADH3*1多态在SCCHN中的重要作用，但需要更多的数字来更准确地估计与ADH3的相互作用。
Squamous cell carcinoma of the head and neck (SCCHN), including the oral cavity, pharynx and larynx, is an excellent tumor model to evaluate gene–environment interactions, including alcohol and alcohol-metabolizing enzymes such as alcohol dehydrogenase (ADH). We conducted a hospital-based case–control study including 182 cases with newly diagnosed SCCHN and 202 controls with non-neoplastic conditions of the head and neck that required surgery. The joint effects of lifetime alcohol use and the presence of theADH3`rapid' allele (ADH3*1) was evaluated in relation to the risk of SCCHN. Logistic regression was used to estimate the interaction between alcohol use andADH3genotype with adjustment for tobacco use, age, sex and race. The interaction was evaluated on both the multiplicative and additive scales. The risk of SCCHN was increased nearly 6-fold with consumption of 40 or more alcoholic beverages per week [odds ratio (OR) = 5.9; 95% confidence interval (CI) = 2.0–17.7; adjusted for age, sex, race and years of tobacco use]. We did not find any increase in risk forADH3*1 homozygotes (OR = 0.9; CI = 0.4–1.9) or heterozygotes (OR = 0.8; CI = 0.4–1.7) relative toADH3*2 homozygotes. There was no suggestion of an interaction between any alcohol use variable and theADH3*1 genotype. For example, the interaction term, including the continuous variable average number of drinks per week and theADH3genotypes, was non-significant (P= 0.22). The study does not indicate an important role for theADH3*1 polymorphism in SCCHN, but larger numbers are needed to more precisely estimate the interaction, if any, withADH3.