期刊
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
卷 63, 期 7, 页码 1143-1150出版社
ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
DOI: 10.1080/01635581.2011.605982
关键词
-
资金
- Western New York Exposures and Breast Cancer (WEB) Study
- National Institute on Alcohol Abuse and Alcoholism [P50-AA09802]
- Department of Defense [DAMD 179616202, DAMD 17030446]
- United States Public Health Service (USPHS) from the National Cancer Institute [R01CA 092040]
- NATIONAL CANCER INSTITUTE [R01CA092040] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [P50AA009802] Funding Source: NIH RePORTER
Aberrant DNA methylation plays a critical role in carcinogenesis, and the availability of dietary factors involved in 1-carbon metabolism may contribute to aberrant DNA methylation. We investigated the association of intake of folate, vitamins B-2, B-6, B-12, and methionine with promoter methylation of E-cadherin, p16, and RAR-beta(2) genes in archived tumor tissues from incident, primary breast cancer cases in a population-based case-control study. Real-time methylation-specific PCR was performed on 803 paraffin-embedded samples; usual dietary intake was queried from a food frequency questionnaire. Unconditional logistic regression was used to derive adjusted odds ratios and 95% confidence intervals for likelihood of promoter methylation for high compared to low intake of those 1-carbon nutrients. Overall, in case-case comparisons, dietary intakes of folate, vitamins B-2, B-6, B-12, and methionine were not associated with likelihood of promoter methylation of E-cadherin, p16, and RAR-beta(2) for all cases combined or within strata defined by menopausal status and estrogen receptor status in this study. This finding, however, does not exclude the possibility that intake of such nutrients might have the ability to modulate promoter methylation in normal or premalignant (dysplastic) breast tissue.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据