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

¹ Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, New York; ² Unit of Genetic Epidemiology, Division of Cancer Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany; and ³ Cancer Genetics and Epidemiology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Northwest, Washington, District of Columbia

Requests for reprints: Christine B. Ambrosone, Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263. Phone: 716-845-3082; Fax: 716-845-8125. E-mail: christine.ambrosone{at}RoswellPark.org

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, P_interaction = 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)

Commentary

Smoking and Breast Cancer: Is There Really a Link?

David H. Phillips and Seymour Garte
Cancer Epidemiol. Biomarkers Prev. 2008 17: 1-2. [Full Text] [PDF]

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				D. H. Phillips and S. Garte Smoking and Breast Cancer: Is There Really a Link? Cancer Epidemiol. Biomarkers Prev., January 1, 2008; 17(1): 1 - 2. [Full Text] [PDF]