The functional <i>ALDH2</i> polymorphism is associated with breast cancer risk: A pooled analysis from the Breast Cancer Association Consortium
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- Tomotaka Ugai
- Division of Cancer Epidemiology and Prevention, Department of Preventive Medicine Aichi Cancer Center Research Institute Nagoya Japan
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- Roger L. Milne
- Cancer Epidemiology & Intelligence Division Melbourne VIC Australia
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- Hidemi Ito
- Division of Cancer Information and Control, Department of Preventive Medicine Aichi Cancer Center Research Institute Nagoya Japan
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- Kristan J. Aronson
- Department of Public Health Sciences Queen's Cancer Institute, Queen's University Kingston Ontario Canada
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- Manjeet K. Bolla
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Tsun Chan
- Hong Kong Hereditary Breast Cancer Family Registry Happy Valley Hong Kong
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- Ching W. Chan
- Department of Surgery National University Health System Singapore
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- Ji‐Yeob Choi
- Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea
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- Don M. Conroy
- Centre for Cancer Genetic Epidemiology, Department of Oncology University of Cambridge Cambridge UK
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- Joe Dennis
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Alison M. Dunning
- Centre for Cancer Genetic Epidemiology, Department of Oncology University of Cambridge Cambridge UK
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- Douglas F. Easton
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Valerie Gaborieau
- Genetic Epidemiology Group, International Agency for Research on Cancer Lyon France
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- Anna Gonzalez‐Neira
- Human Cancer Genetics Program Spanish National Cancer Research Centre Madrid Spain
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- Mikael Hartman
- Department of Surgery National University Health System Singapore
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- Catherine S. Healey
- Centre for Cancer Genetic Epidemiology, Department of Oncology University of Cambridge Cambridge UK
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- Motoki Iwasaki
- Epidemiology and Prevention Group, Center for Public Health Sciences National Cancer Center Tokyo Japan
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- Esther M. John
- Department of Medicine and Stanford Cancer Institute Stanford University School of Medicine Stanford California USA
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- Daehee Kang
- Department of Biomedical Sciences Seoul National University College of Medicine Seoul Korea
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- Sung‐Won Kim
- Department of Surgery Daerim Saint Mary's Hospital Seoul Korea
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- Ava Kwong
- Hong Kong Hereditary Breast Cancer Family Registry Happy Valley Hong Kong
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- Artitaya Lophatananon
- Division of Health Sciences, Warwick Medical School Warwick University Coventry UK
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- Kyriaki Michailidou
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Nur Aishah Mohd Taib
- Breast Cancer Research Unit University Malaya Cancer Research Institute, University Malaya Medical Centre Kuala Lumpur Malaysia
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- Kenneth Muir
- Division of Health Sciences, Warwick Medical School Warwick University Coventry UK
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- Sue K. Park
- Department of Preventive Medicine Seoul National University College of Medicine Seoul Korea
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- Paul D. P. Pharoah
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Suleeporn Sangrajrang
- National Cancer Institute Bangkok Thailand
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- Chen‐Yang Shen
- Taiwan Biobank Institute of Biomedical Sciences, Academia Sinica Taipei Taiwan
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- Xiao‐Ou Shu
- Division of Epidemiology, Department of Medicine Vanderbilt Epidemiology Center, Vanderbilt‐Ingram Cancer Center, Vanderbilt University School of Medicine Nashville Tennessee USA
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- John J. Spinelli
- School of Population & Public Health University of British Columbia Vancouver British Columbia Canada
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- Soo H. Teo
- Breast Cancer Research Unit University Malaya Cancer Research Institute, University Malaya Medical Centre Kuala Lumpur Malaysia
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- Daniel C. Tessier
- McGill University and Génome Québec Innovation Centre Montreal Quebec Canada
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- Chiu‐Chen Tseng
- Department of Preventive Medicine, Keck School of Medicine University of Southern California Los Angeles California USA
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- Shoichiro Tsugane
- Epidemiology and Prevention Group, Center for Public Health Sciences National Cancer Center Tokyo Japan
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- Daniel Vincent
- McGill University and Génome Québec Innovation Centre Montreal Quebec Canada
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- Qin Wang
- Centre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care University of Cambridge Cambridge UK
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- Anna H. Wu
- Department of Preventive Medicine, Keck School of Medicine University of Southern California Los Angeles California USA
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- Pei‐Ei Wu
- Taiwan Biobank Institute of Biomedical Sciences, Academia Sinica Taipei Taiwan
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- Wei Zheng
- Division of Epidemiology, Department of Medicine Vanderbilt Epidemiology Center, Vanderbilt‐Ingram Cancer Center, Vanderbilt University School of Medicine Nashville Tennessee USA
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- Keitaro Matsuo
- Division of Cancer Epidemiology and Prevention, Department of Preventive Medicine Aichi Cancer Center Research Institute Nagoya Japan
Description
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Epidemiological studies consistently indicate that alcohol consumption is an independent risk factor for female breast cancer (BC). Although the aldehyde dehydrogenase 2 (<jats:italic>ALDH2</jats:italic>) polymorphism (rs671: Glu>Lys) has a strong effect on acetaldehyde metabolism, the association of rs671 with BC risk and its interaction with alcohol intake have not been fully elucidated. We conducted a pooled analysis of 14 case‐control studies, with individual data on Asian ancestry women participating in the Breast Cancer Association Consortium.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>We included 12,595 invasive BC cases and 12,884 controls for the analysis of rs671 and BC risk, and 2,849 invasive BC cases and 3,680 controls for the analysis of the gene‐environment interaction between rs671 and alcohol intake for BC risk. The pooled odds ratios (OR) with 95% confidence intervals (CI) associated with rs671 and its interaction with alcohol intake for BC risk were estimated using logistic regression models.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>The Lys/Lys genotype of rs671 was associated with increased BC risk (OR = 1.16, 95% CI 1.03–1.30, <jats:italic>p</jats:italic> = 0.014). According to tumor characteristics, the Lys/Lys genotype was associated with estrogen receptor (ER)‐positive BC (OR = 1.19, 95% CI 1.05–1.36, <jats:italic>p</jats:italic> = 0.008), progesterone receptor (PR)‐positive BC (OR = 1.19, 95% CI 1.03–1.36, <jats:italic>p</jats:italic> = 0.015), and human epidermal growth factor receptor 2 (HER2)‐negative BC (OR = 1.25, 95% CI 1.05–1.48, <jats:italic>p</jats:italic> = 0.012). No evidence of a gene‐environment interaction was observed between rs671 and alcohol intake (<jats:italic>p</jats:italic> = 0.537).</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>This study suggests that the Lys/Lys genotype confers susceptibility to BC risk among women of Asian ancestry, particularly for ER‐positive, PR‐positive, and HER2‐negative tumor types.</jats:p></jats:sec>
Journal
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- Molecular Genetics & Genomic Medicine
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Molecular Genetics & Genomic Medicine 7 (6), 2019-05-07
Wiley
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Keywords
Details 詳細情報について
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- CRID
- 1361131414704756864
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- DOI
- 10.1002/mgg3.707
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- ISSN
- 23249269
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- Data Source
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- Crossref
- KAKEN