| Autor: |
Chevrier, Cécile, Bahuau, Michel, Perret, Claire, Iovannisci, David M., Nelva, Agnès, Herman, Christine, Vazquez, MariePaule, Francannet, Christine, RobertGnansia, Elisabeth, Lammer, Edward J., Cordier, Sylvaine |
| Zdroj: |
American Journal of Medical Genetics. Part A; September 2008, Vol. 146 Issue: 18 p2396-2406, 11p |
| Abstrakt: |
Maternal tobacco consumption is considered as a risk factor for nonsyndromic oral clefts. However, this risk is moderate and may be modulated by genetic susceptibilities, including variants of the TGFA, TGFB3and MSX1developmental genes and polymorphisms of genes of the CYP1A1, 2E1 and GSTM1, T1 families involved in metabolic pathways of tobacco smoke compounds. This French case–control study 1998–2001; 240 nonsyndromic cases, 236 controls included a caseparent design 175 triadfamilies that made it possible to distinguish the direct effect of the childs genotype and maternally mediated effects. Maternal smoking during the first trimester of pregnancy was not associated with the oral cleft risk in this population, but we observed statistically significant increased risks associated with maternal exposure to environmental tobacco smoke ETS. No variant of any of the three developmental genes was significantly associated with oral cleft. The fetal CYP1A12Cvariant allele was associated with a statistically significant decreased risk, compared with the homozygous wildtype: relative risk 0.48, 95 confidence interval: 0.2, 1.0. Suggestive reduced risks were also observed for the maternal CYP1A12Callele and the fetal CYP2E15allele. The GSTM1and GSTT1deletions appeared to play no role. Our findings suggest some interactions, with the strongest between ETS and CYP1A1or MSX1and between maternal smoking and CYP2E1. We did not confirm the maternal smokinginfant GSTT1null interaction previously reported by other investigators. © 2008 WileyLiss, Inc. |
| Databáze: |
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