BREAST-CANCER RISK, MEAT CONSUMPTION AND N-ACETYLTRANSFERASE (NAT2) GENETIC POLYMORPHISMS

Citation
Cb. Ambrosone et al., BREAST-CANCER RISK, MEAT CONSUMPTION AND N-ACETYLTRANSFERASE (NAT2) GENETIC POLYMORPHISMS, International journal of cancer, 75(6), 1998, pp. 825-830
Citations number
28
Categorie Soggetti
Oncology
ISSN journal
00207136
Volume
75
Issue
6
Year of publication
1998
Pages
825 - 830
Database
ISI
SICI code
0020-7136(1998)75:6<825:BRMCAN>2.0.ZU;2-I
Abstract
Although inconsistencies exist, some studies have shown that meat cons umption is associated with breast cancer risk. Several heterocyclic am ines (HAs), formed in the cooking of meats, are mammary carcinogens in laboratory models. HAs are activated by polymorphic N-acetyltransfera se (NAT2) and rapid NAT2 activity may increase risk associated with HA s. We investigated whether ingestion of meat, chicken and fish, as wel l as particular concentrated sources of HAs, was associated with breas t cancer risk, and if NAT2 genotype modified risk. Caucasian women wit h incident breast cancer (n = 740) and community controls (n = 810) we re interviewed and administered a food frequency questionnaire. A subs et of these women (n = 793) provided a blood sample. Polymerase chain reaction and restriction fragment length polymorphism analyses were us ed to determine NAT2 genotype. Consumption of red meats, as well as an index of concentrated sources of HAs, was not associated with increas ed breast cancer risk, nor did risk vary by NAT2 genotype. In post-men opausal women, higher fish consumption was inversely associated with r isk (odds ratio = 0.7; 95% confidence interval, 0.4-1.0); among pre-me nopausal women, there was the suggestion of inverse associations betwe en risk and pork and chicken intake. Our results suggest that consumpt ion of meats and other concentrated sources of HAs is not associated w ith 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 stud y, further studies of these possible relationships are warranted. (C) 1998 Wiley-Liss, Inc.