Heterocyclic amines (HAs) are carcinogens produced by high-temperature cooking of meat and animal protein; metabolism of HA is influenced by polymorphisms in the Nacetyltransferase-2 (NAT-2) gene. Data from a variety of sources suggest that HA may play a role in human carcinogenesis. We examined the
Breast cancer risk, meat consumption and N-acetyltransferase (NAT2) genetic polymorphisms
β Scribed by Christine B. Ambrosone; Jo L. Freudenheim; Rashmi Sinha; Saxon Graham; James R. Marshall; John E. Vena; Rosemary Laughlin; Takuma Nemoto; Peter G. Shields
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- French
- Weight
- 53 KB
- Volume
- 75
- Category
- Article
- ISSN
- 0020-7136
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β¦ Synopsis
Although inconsistencies exist, some studies have shown that meat consumption is associated with breast cancer risk. Several heterocyclic amines (HAs), formed in the cooking of meats, are mammary carcinogens in laboratory models. HAs are activated by polymorphic N-acetyltransferase (NAT2) and rapid NAT2 activity may increase risk associated with HAs. We investigated whether ingestion of meat, chicken and fish, as well as particular concentrated sources of HAs, was associated with breast cancer risk, and if NAT2 genotype modified risk. Caucasian women with incident breast cancer (n Ο 740) and community controls (n Ο 810) were interviewed and administered a food frequency questionnaire. A subset of these women (n Ο 793) provided a blood sample. Polymerase chain reaction and restriction fragment length polymorphism analyses were used to determine NAT2 genotype. Consumption of red meats, as well as an index of concentrated sources of HAs, was not associated with increased breast cancer risk, nor did risk vary by NAT2 genotype. In post-menopausal women, higher fish consumption was inversely associated with risk (odds ratio Ο 0.7; 95% confidence interval, 0.4-1.0); among pre-menopausal women, there was the suggestion of inverse associations between risk and pork and chicken intake. Our results suggest that consumption of meats and other concentrated sources of HAs is not associated with increased breast cancer risk. However, due to the strong biologic plausibility for a role of some HAs in mammary carcinogenesis, and the likely measurement error in evaluation of sources of HAs in this study, further studies of these possible relationships are warranted.
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