Genetic susceptibility to breast cancer in French-Canadians: role of carcinogen-metabolizing enzymes and gene-environment interactions. Krajinovic, M., Ghadirian, P., Richer, C., Sinnett, H., Gandini, S., Perret, C., Lacroix, A., Labuda, D., & Sinnett, D. Int J Cancer, 92(2):220-5., 2001.
abstract   bibtex   
Breast cancer is the most frequent malignancy among women. Since genetic factors such as BRCA1 and BRCA2 as well as reproductive history constitute only 30% of the cause, environmental exposure may play a significant role in the development of breast cancer. Likewise, the relevant enzymes involved in the biotransformation of xenobiotics (from tobacco smoke, diet or other environmental sources) might play a role in breast carcinogenesis. Since individuals with modified ability to metabolize these carcinogens could have a different risk for breast cancer, we investigated the role of cytochromes P-450 (CYP1A1, CYP2D6), glutathione-S-transferases (GSTM1, GSTT1, GSTP1) and N-acetyltransferases (NAT1, NAT2) gene variants in breast carcinogenesis. A case-control study was conducted on 149 women with breast carcinoma and 207 healthy controls, both of French-Canadian origin. The CYP1A1*4 allele was found to be a significant risk determinant of breast carcinoma (OR = 3.3, 95% CI 1.1-9.7), particularly among post-menopausal women (OR = 4.0, 95% CI 1.2-13.8). The frequency of NAT2 rapid acetylators was increased among smokers (OR = 2.6, 95% CI 0.8-8.2), while the NAT1*10 allele conferred a 4-fold increase in risk among women who consumed well-done meat (OR = 4.4, 95% CI 1.0-18.9). These data suggest that CYP1A1*4, NAT1 and NAT2 variants are involved in the susceptibility to breast carcinoma by modifying the impact of exogenous and/or endogenous exposures. Copyright 2001 Wiley-Liss, Inc.
@article{
 title = {Genetic susceptibility to breast cancer in French-Canadians: role of carcinogen-metabolizing enzymes and gene-environment interactions},
 type = {article},
 year = {2001},
 identifiers = {[object Object]},
 keywords = {*Genetic Predisposition to Disease,Arylamine N-Acetyltransferase/genetics,Breast Neoplasms/*enzymology/epidemiology/*genetic,Canada/epidemiology,Carcinogens/*metabolism,Carcinoma/*enzymology/epidemiology/*genetics,Case-Control Studies,Cytochrome P-450 CYP1A1/genetics,Cytochrome P-450 CYP2D6/genetics,Environmental Exposure,Female,France/ethnology,Gene Frequency,Genotype,Glutathione Transferase/genetics,Human,Isoenzymes/genetics,Menopause,Middle Age,Polymorphism (Genetics),Risk Factors,Support, Non-U.S. Gov't},
 pages = {220-5.},
 volume = {92},
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 abstract = {Breast cancer is the most frequent malignancy among women. Since genetic factors such as BRCA1 and BRCA2 as well as reproductive history constitute only 30% of the cause, environmental exposure may play a significant role in the development of breast cancer. Likewise, the relevant enzymes involved in the biotransformation of xenobiotics (from tobacco smoke, diet or other environmental sources) might play a role in breast carcinogenesis. Since individuals with modified ability to metabolize these carcinogens could have a different risk for breast cancer, we investigated the role of cytochromes P-450 (CYP1A1, CYP2D6), glutathione-S-transferases (GSTM1, GSTT1, GSTP1) and N-acetyltransferases (NAT1, NAT2) gene variants in breast carcinogenesis. A case-control study was conducted on 149 women with breast carcinoma and 207 healthy controls, both of French-Canadian origin. The CYP1A1*4 allele was found to be a significant risk determinant of breast carcinoma (OR = 3.3, 95% CI 1.1-9.7), particularly among post-menopausal women (OR = 4.0, 95% CI 1.2-13.8). The frequency of NAT2 rapid acetylators was increased among smokers (OR = 2.6, 95% CI 0.8-8.2), while the NAT1*10 allele conferred a 4-fold increase in risk among women who consumed well-done meat (OR = 4.4, 95% CI 1.0-18.9). These data suggest that CYP1A1*4, NAT1 and NAT2 variants are involved in the susceptibility to breast carcinoma by modifying the impact of exogenous and/or endogenous exposures. Copyright 2001 Wiley-Liss, Inc.},
 bibtype = {article},
 author = {Krajinovic, M and Ghadirian, P and Richer, C and Sinnett, H and Gandini, S and Perret, C and Lacroix, A and Labuda, D and Sinnett, D},
 journal = {Int J Cancer},
 number = {2}
}

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