期刊
INTERNATIONAL JOURNAL OF CANCER
卷 148, 期 6, 页码 1338-1350出版社
WILEY
DOI: 10.1002/ijc.33308
关键词
alcohol intake; breast cancer; causal inference; Mendelian randomization; ovarian cancer
类别
资金
- National Health and Medical Research Council [1123248]
- UK Biobank Resource [25331]
- Cancer Genome Atlas Pilot Project [phs000178.v8.p7]
- Wellcome Trust Case Control consortium [076113]
- US National Cancer Institute GAME-ON Post-GWAS Initiative [U19-CA148112]
- European Union [H2020 634935, H2020 633784, HEALTH-F2-2009-223175]
- Cancer Research UK [C1287/A10710, C1287/A16563, C1287/A10118]
- National Institutes of Health [X01HG007492, U19 CA148065]
- Ministere de l'Economie, de la Science et de l'Innovation du Quebec [PSR-SIIRI-701]
- National Health and Medical Research Council of Australia [1123248] Funding Source: NHMRC
Alcohol consumption is positively correlated with the risk of breast cancer according to observational studies and genetic analysis, while the association with epithelial ovarian cancer remains inconclusive. The findings indicate a small effect of alcohol intake on the risk of these cancers, consistent with previous research by the World Cancer Research Fund.
Alcohol consumption is correlated positively with risk for breast cancer in observational studies, but observational studies are subject to reverse causation and confounding. The association with epithelial ovarian cancer (EOC) is unclear. We performed both observational Cox regression and two-sample Mendelian randomization (MR) analyses using data from various European cohort studies (observational) and publicly available cancer consortia (MR). These estimates were compared to World Cancer Research Fund (WCRF) findings. In our observational analyses, the multivariable-adjusted hazard ratios (HR) for a one standard drink/day increase was 1.06 (95% confidence interval [CI]; 1.04, 1.08) for breast cancer and 1.00 (0.92, 1.08) for EOC, both of which were consistent with previous WCRF findings. MR ORs per genetically predicted one standard drink/day increase estimated via 34 SNPs using MR-PRESSO were 1.00 (0.93, 1.08) for breast cancer and 0.95 (0.85, 1.06) for EOC. Stratification by EOC subtype or estrogen receptor status in breast cancers made no meaningful difference to the results. For breast cancer, the CIs for the genetically derived estimates include the point-estimate from observational studies so are not inconsistent with a small increase in risk. Our data provide additional evidence that alcohol intake is unlikely to have anything other than a very small effect on risk of EOC.
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