N-acetyltransferase 2 polymorphism and breast cancer risk with smoking: a case control study in Japanese women

• Published in: Breast cancer (Tokyo, Japan) Japan), 2017-03, Vol.24 (2), p.254-262
• Main Authors: Hara, Akio, Taira, Naruto, Mizoo, Taeko, Nishiyama, Keiko, Nogami, Tomohiro, Iwamoto, Takayuki, Motoki, Takayuki, Shien, Tadahiko, Matsuoka, Junji, Doihara, Hiroyoshi, Ishihara, Setsuko, Kawai, Hiroshi, Kawasaki, Kensuke, Ishibe, Youichi, Ogasawara, Yutaka, Miyoshi, Shinichiro
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aged, 80 and over; Arylamine N-Acetyltransferase - genetics; Asian Continental Ancestry Group - genetics; Breast cancer; Breast Neoplasms - genetics; Cancer; Cancer Research; Case-Control Studies; Female; Gene Frequency; Genetic aspects; Genetic polymorphisms; Genetic Predisposition to Disease; Health aspects; Humans; Medicine; Medicine & Public Health; Middle Aged; Oncology; Oncology, Experimental; Original Article; Polymorphism, Single Nucleotide; Risk factors; Smoking - adverse effects; Smoking - genetics; Surgery; Surgical Oncology
• ISSN: 1340-6868; 1880-4233
• DOI: 10.1007/s12282-016-0696-1

Background Recent studies have suggested that the association between smoking and breast cancer risk might be modified by polymorphisms in the N -acetyltransferase 2 gene (NAT2). Most of these studies were conducted in Western countries, with few reports from East Asia. Methods We conducted a case–control study of 511 breast cancer cases and 527 unmatched healthy controls from December 2010 to November 2011 in Japan. Unconditional logistic regression was used to analyze the association of smoking with breast cancer risk stratified by NAT2 phenotype. Results In this population, 11 % of the cases and 10 % of the controls were classified as a slow acetylator phenotype. Compared to never smokers, current smokers had an increased breast cancer risk in multivariate analysis [odds ratio (OR) = 2.27, 95 % confidence interval (95 %CI) = 1.38–3.82]. Subgroup analyses of menopausal status indicated the same tendency. Subgroup analyses of NAT2 phenotype, the ORs in both of rapid and slow acetylator phenotype subgroups were comparable, and no interactions were observed between smoking status and NAT2 phenotype ( p  = 0.97). A dose-dependent effect of smoking on breast cancer risk was seen for the rapid acetylator phenotype, but not for the slow acetylator phenotype. Conclusion Given the high frequency of the rapid acetylator phenotype, these results show that smoking is a risk factor for breast cancer among most Japanese women. It may be of little significance to identify the NAT2 phenotype in the Japanese population.