Oral clefts, maternal smoking, and TGFA: A meta-analysis of gene-environment interaction
Oral clefts, maternal smoking, and TGFA: A meta-analysis of gene-environment interaction
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DOI：
10.1597/02-128.1
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Liang, KY
中科院分区：
文献类型：
--
作者：
Zeiger, JS;Beaty, TH;Liang, KY
目的：通过荟萃分析，探讨母亲吸烟、婴儿转化生长因子α (TGFA)基因座Taq1位点基因型与非综合征性唇裂、腭裂（CP）和唇裂伴或不伴腭裂（CUP）风险之间的关系。设计：荟萃分析纳入了5项已发表的病例对照研究。计算合并的Mantel-Haenszel优势比（OR）和95%置信区间（CIs）。基因与环境的相互作用也通过个案分析和多元逻辑回归的汇总数据进行评估。结果：在不吸烟的母亲中，没有证据表明婴儿携带TGFA Taq1 C2等位基因会增加患CP的风险。然而，如果母亲报告吸烟，如果婴儿携带C2等位基因，则患CP的总体风险增加（吸烟者= 1.95;95% Cl = 1.22至3.10）。无论母亲是否吸烟，TGFA基因型均不会增加患CUP的风险。多元logistic回归显示，吸烟对CUP （OR = 1.64, 95% Cl = 1.33 ~ 2.02）和CP （OR = 1.42, 95% Cl = 1.06 ~ 1.90）的总体影响显著。结论：虽然在所有研究中，母亲吸烟都是导致CUP和CP的一个一致的危险因素，但婴儿TGFA中Taq1标记基因型与母亲吸烟之间的基因-环境相互作用的暗示证据仅限于CP。此外，这种基因-环境相互作用的证据在一项来自出生缺陷登记处的病例对照研究中最为明显，该研究以无唇裂缺陷的婴儿为对照。
Objective: A meta-analysis was performed to examine the association among maternal cigarette smoking, infant genotype at the Taq1 site in the transforming growth factor alpha (TGFA) locus, and risk of nonsyndromic oral clefts, both cleft palate (CP) and cleft lip with or without cleft palate (CUP).Design: Five published case-control studies were included in the meta-analyis. Pooled Mantel-Haenszel odds ratios (OR) and 95% confidence intervals (CIs) were computed. Gene-environment interaction was also assessed by using the pooled data in a case-only analysis and polytomous logistic regression.Results: Among nonsmoking mothers, there was no evidence of any increased risk for CP if the infant carried the TGFA Taq1 C2 allele. If the mother reported smoking, however, there was an overall increased risk for CP if the infant carried the C2 allele (ORsmokers = 1.95; 95% Cl = 1.22 to 3.10). TGFA genotype did not increase risk to CUP, regardless of maternal smoking status. Polytomous logistic regression revealed a significant overall smoking effect for CUP (OR = 1.64, 95% Cl = 1.33 to 2.02) and CP (OR = 1.42, 95% Cl = 1.06 to 1.90).Conclusions: While maternal smoking was a consistent risk factor for both CUP and CP across all studies, the suggestive evidence for gene-environment interaction between the infant's genotype at the Taq1 marker in TGFA and maternal smoking was limited to CP. Furthermore, evidence for such gene-environment interaction was strongest in a case-control study drawn from a birth defect registry where infants with non-cleft defects served as controls.