Carcinogenesis Advance Access originally published online on January 23, 2004
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Carcinogenesis, Vol. 25, No. 6, 931-939,
June 2004
Carcinogenesis vol.25 no.6 © Oxford University Press 2004; all rights reserved.
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Diet and alcohol consumption in relation to p53 mutations in breast tumors
1 Department of Social and Preventive Medicine, University at Buffalo, Buffalo, NY 14214, USA, 2 Lombardi Cancer Center, Georgetown University, Washington, DC 20007, USA, 3 Roswell Park Cancer Institute, Buffalo, NY 14263, USA, 4 Laboratory for Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland, USA and 5 Department of Surgery, University at Buffalo, Buffalo, NY 14214, USA
6 To whom correspondence should be addressed Email: Jfreuden{at}buffalo.edu
7To whom correspondence may also be addressed Email: pgs2{at}georgetown.edu
There is evidence linking alcohol consumption to p53 mutations in tumors, considerable evidence linking alcohol consumption with risk of breast cancer and some evidence that alcohol and folate consumption interact to affect risk. Further, while there is some indication that oxidation may play a role in breast cancer etiology, there has been little examination of an association of oxidative stress with p53 mutations. We examined several dietary components related to one-carbon metabolism and antioxidants to determine if these factors were related to the prevalence of p53 mutations in breast tumors. We conducted a case-control study of primary, histologically confirmed breast cancer in western New York. Controls <65 were selected from drivers license lists; those 
65 were selected from Health Care Finance Administration lists. p53 mutations in archived tumor blocks were identified in exons 2–11 and flanking intron sequences. Usual dietary intake was assessed by interview regarding intake in the previous 2 years; alcohol consumption was queried for 2, 10 and 20 years in the past. Our data were consistent with increased likelihood of tumors with p53 mutations for premenopausal breast cancer with increased alcohol intake 10 or 20 years previous; for intake of 16 or more drinks per month in the period 20 years before the interview compared with non-drinkers, the OR was 5.25, 95% CI 1.48–18.58. For postmenopausal women, there was increased likelihood of tumors with p53 mutations among women with higher folate. Antioxidant nutrients were not differentially related to p53 mutations. These results indicate that there may be heterogeneity in breast tumors, as indicated by differences in associations for those with or without p53 mutations, and that causal pathways for these nutrients may vary for pre- and postmenopausal women. For premenopausal women, alcohol consumption in the past was associated with p53 mutations.
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