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Cancer Epidemiology, Biomarkers & Prevention
Cancer Epidemiology, Biomarkers & Prevention
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Cigarette Smoking, N-Acetyltransferase 2 Genotypes, and Breast Cancer Risk: Pooled Analysis and Meta-analysis

Christine B. Ambrosone, Silke Kropp, Jun Yang, Song Yao, Peter G. Shields and Jenny Chang-Claude
Christine B. Ambrosone
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Silke Kropp
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Jun Yang
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Song Yao
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Peter G. Shields
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Jenny Chang-Claude
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DOI: 10.1158/1055-9965.EPI-07-0598 Published January 2008
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Abstract

Approximately 10 years ago, it was noted that smoking increased risk of breast cancer among women with N-acetyltransferase 2 (NAT2) slow acetylation genotypes. This report was followed by a number of studies to address this question. We pooled data from 10 existing studies and also conducted a meta-analysis of 13 studies published from 1996 to October 2006 that were conducted among women, were published in English, and had adequate information on smoking and NAT2 genotyping. Raw data were requested from authors. Unconditional logistic regression was done for pooled analysis, and random effect models was done for meta-analysis. Study heterogeneity was assessed, and sensitivity tests were done when subgroups were excluded from the analysis. In the pooled analysis, there was a significant interaction between smoking, NAT2 genotype, and risk of breast cancer [pack-years (continuous variable, Pinteraction = 0.03)], with higher pack-years significantly associated with an increased risk of breast cancer among women with NAT2 slow genotypes (pooled analysis relative risk, 1.49; 95% confidence interval, 1.08-2.04). These findings were supported by the meta-analysis including all studies; pack-years were significantly associated with risk among slow acetylators in a dose-dependent fashion (meta-analysis relative risk, 1.44; 95% confidence interval, 1.23-1.68 for ≥20 pack-years versus never smokers), but not among rapid acetylators. Similar relationships were noted for smoking status (ever, never) and duration of smoking. Our results show that cigarette smoking is associated with an increase in breast cancer risk among women with NAT2 slow acetylation genotypes. Because slow NAT2 genotypes are present in 50% to 60% of Caucasian populations, smoking is likely to play an important role in breast cancer etiology. (Cancer Epidemiol Biomarkers Prev 2008;17(1):15–26)

  • breast cancer
  • cigarette smoking
  • N-acetyltransferase 2
  • genetic polymorphism
  • gene-environment interactions

Footnotes

  • The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted September 25, 2007.
    • Received June 30, 2007.
    • Revision received September 19, 2007.
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Cancer Epidemiology Biomarkers & Prevention: 17 (1)
January 2008
Volume 17, Issue 1
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Cigarette Smoking, N-Acetyltransferase 2 Genotypes, and Breast Cancer Risk: Pooled Analysis and Meta-analysis
Christine B. Ambrosone, Silke Kropp, Jun Yang, Song Yao, Peter G. Shields and Jenny Chang-Claude
Cancer Epidemiol Biomarkers Prev January 1 2008 (17) (1) 15-26; DOI: 10.1158/1055-9965.EPI-07-0598

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Cigarette Smoking, N-Acetyltransferase 2 Genotypes, and Breast Cancer Risk: Pooled Analysis and Meta-analysis
Christine B. Ambrosone, Silke Kropp, Jun Yang, Song Yao, Peter G. Shields and Jenny Chang-Claude
Cancer Epidemiol Biomarkers Prev January 1 2008 (17) (1) 15-26; DOI: 10.1158/1055-9965.EPI-07-0598
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