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N-Acetyltransferase (NAT2) Polymorphism and Breast Cancer Susceptibility: A Lack of Association in a Case-Control Study of Turkish Population

Lookup NU author(s): Emerita Professor Suzanne Cholerton, Professor Ann DalyORCiD


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Increased exposure to environmental carcinogens, including several aromatic and heterocyclic amines (HAs), is suspected to be one factor contributing to incidence of breast cancer. The N-acetyltransferase 2 (NAT2) acetylation polymorphism have been associated with a number of drug-induced toxicities and cancer in various tissues, resulting from decreased capacity to activate/deactivate several aromatic amine, hydrazine drugs, as well as HA carcinogens. Ethnic differences exist in NAT2 genotype frequencies, which may be a factor in cancer incidence. Our present case-control study in Turkey was performed to explore the association between NAT2 genetic polymorphism and individual susceptibility to breast cancer. The NAT2 genotypes (*4, *12A, *5A, *5B, *5C, *6, *7) were determined using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in 84 breast cancer patients and 103 healthy controls, and 50% and 56.3%, respectively, were found to be slow acetylator genotypes. There was no significant difference in risk for breast cancer development among patients with rapid and slow acetylators, with adjusted odds ratio 0.78 (95% confidence interval 0.44 to 1.38). Also, risk was not affected by different variables. To our knowledge, this is the first genetic study on the association of NAT2 genotypes with breast cancer in the Turkish population, and this finding showed that NAT2 polymorphism does not play an important role in breast cancer risk of Turkish women by altering the capacity in deactivation of environmental carcinogens, even though small sample size and wide confidence interval.

Publication metadata

Author(s): Kocabas NA, Sardas S, Cholerton S, Daly AK, Karakaya AE

Publication type: Article

Publication status: Published

Journal: International Journal of Toxicology

Year: 2004

Volume: 23

Issue: 1

Pages: 25-31

ISSN (print): 1091-5818

ISSN (electronic): 1092-874X

Publisher: Sage


DOI: 10.1080/10915810490275053

PubMed id: 15162844


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