...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Alcohol >Alcohol consumption in relation to aberrant DNA methylation in breast tumors
【24h】

Alcohol consumption in relation to aberrant DNA methylation in breast tumors

机译：饮酒与乳腺肿瘤中异常的DNA甲基化有关

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The mechanism for the observed association of alcohol consumption breast cancer risk is not known; understanding that mechanism could improve understanding of breast carcinogenesis and optimize prevention strategies. Alcohol may impact breast malignancies or tumor progression by altering DNA methylation. We examined promoter methylation of three genes, the E-cadherin, p16, and retinoic acid-binding receptor-β 2 (RAR-β 2) genes in archived breast tumor tissues from participants in a population-based case-control study. Real time methylation-specific PCR was performed on 803 paraffin-embedded samples, and lifetime alcohol consumption was queried. Unordered polytomous and unconditional logistic regression were used to derive adjusted odds ratios (ORs) and 95% confidence intervals (CIs). RAR-β 2 methylation was not associated with drinking. Among premenopausal women, alcohol consumption was also not associated with promoter methylation for E-cadherin and p16 genes. In case-case comparisons of postmenopausal breast cancer, compared with lifetime never drinkers, promoter methylation likelihood was increased for higher alcohol intake for E-cadherin (OR=2.39; 95% CI, 1.15-4.96), in particular for those with estrogen receptor-negative tumors (OR=4.13; 95% CI, 1.16-14.72), and decreased for p16 (OR=0.52; 95% CI, 0.29-0.92). There were indications that the association with p16 was stronger for drinking at younger ages. Methylation was also associated with drinking intensity independent of total consumption for both genes. We found alcohol consumption was associated with DNA methylation in postmenopausal breast tumors, suggesting that the association of alcohol and breast cancer may be related, at least in part, to altered methylation, and may differ by drinking pattern.
机译：酒精摄入与乳腺癌风险之间存在相关性的机制尚不清楚。了解这种机制可以增进对乳腺癌致癌作用的了解并优化预防策略。酒精可能会通过改变DNA甲基化影响乳房恶性肿瘤或肿瘤进展。在一项基于人群的病例对照研究中，我们检查了已归档的乳腺肿瘤组织中三个基因（E-钙粘蛋白，p16和视黄酸结合受体-β2（RAR-β2））的启动子甲基化。对803个石蜡包埋的样品进行了实时甲基化特异性PCR，并查询了终生饮酒量。使用无序多变量和无条件逻辑回归来得出调整后的优势比（OR）和95％置信区间（CI）。 RAR-β2甲基化与饮酒无关。在绝经前妇女中，饮酒也与E-cadherin和p16基因的启动子甲基化无关。在绝经后乳腺癌的病例-病例比较中，与终身不饮酒的人相比，E-钙黏着蛋白摄入更多酒精（OR = 2.39; 95％CI，1.15-4.96）时，启动子甲基化的可能性增加，特别是对于那些具有雌激素受体的人-阴性肿瘤（OR = 4.13; 95％CI，1.16-14.72），p16减少（OR = 0.52; 95％CI，0.29-0.92）。有迹象表明，与p16的关联性在年纪较小的人中更强。甲基化还与饮酒强度相关，而与两个基因的总消耗量无关。我们发现饮酒与绝经后乳腺肿瘤中的DNA甲基化有关，这表明酒精与乳腺癌的联系可能至少部分与甲基化改变有关，并且可能因饮酒方式而异。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号