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LEP、LEPR、ADIPOQ、ADIPOR1或ADIPOR2基因多态性与绝经后乳腺癌风险之间无关联。

No association between polymorphisms in LEP, LEPR, ADIPOQ, ADIPOR1, or ADIPOR2 and postmenopausal breast cancer risk.

作者信息

Teras Lauren R, Goodman Michael, Patel Alpa V, Bouzyk Mark, Tang Weining, Diver W Ryan, Feigelson Heather Spencer

机构信息

Department of Epidemiology, American Cancer Society, National Home Office, 250 Williams Street Northwest, Atlanta, GA 30303, USA.

出版信息

Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2553-7. doi: 10.1158/1055-9965.EPI-09-0542. Epub 2009 Sep 1.

DOI:10.1158/1055-9965.EPI-09-0542
PMID:19723917
Abstract

There is evidence that adipokines such as leptin and adiponectin may influence breast tumor development. We conducted a nested case-control study using women in the American Cancer Society Cancer Prevention Study II to examine the association between postmenopausal breast cancer and variability in the genes encoding leptin, the leptin receptor, adiponectin, adiponectin receptor 1, and adiponectin receptor 2. Using 648 cases and 659 controls, we found no statistically significant (P < 0.05) associations between breast cancer risk and any of the single nucleotide polymorphisms. Individual odds ratios ranged from 0.93 to 1.06. We found no evidence of effect modification by body mass index, adult weight gain, location of weight gain, or physical activity. Although we cannot rule out that these genes are involved in gene-gene or gene-environment interactions, our results suggest that individual single nucleotide polymorphisms in these genes do not substantially affect postmenopausal breast cancer risk.

摘要

有证据表明,瘦素和脂联素等脂肪因子可能会影响乳腺肿瘤的发展。我们利用美国癌症协会癌症预防研究II中的女性进行了一项巢式病例对照研究,以检验绝经后乳腺癌与编码瘦素、瘦素受体、脂联素、脂联素受体1和脂联素受体2的基因变异之间的关联。通过648例病例和659例对照,我们发现乳腺癌风险与任何单核苷酸多态性之间均无统计学显著关联(P < 0.05)。个体比值比范围为0.93至1.06。我们没有发现体重指数、成年期体重增加、体重增加部位或身体活动对效应产生修饰作用的证据。虽然我们不能排除这些基因参与基因-基因或基因-环境相互作用,但我们的结果表明,这些基因中的个体单核苷酸多态性不会实质性影响绝经后乳腺癌风险。

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