Vegetable, fruit and meat consumption and potential risk modifying genes in relation to colorectal cancer

被引:54
作者
Turner, F
Smith, G
Sachse, C
Lightfoot, T
Garner, RC
Wolf, CR
Forman, D
Bishop, DT
Barrett, JH
机构
[1] St James Univ Hosp, Canc Res UK Clin Ctr, Genet Epidemiol Div, Leeds LS9 7TF, W Yorkshire, England
[2] Canc Res UK Mol Pharmacol Unit, Dundee, Scotland
[3] Univ York, York YO10 5DD, N Yorkshire, England
[4] Univ Leeds, Leeds, W Yorkshire, England
关键词
diet; colorectal cancer; metabolic polymorphisms;
D O I
10.1002/ijc.20404
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epidemiological evidence shows high red meat consumption to increase the risk of colorectal cancer, while the consumption of fruit and vegetables has been shown to be protective. Many genes have been identified that encode for enzymes involved in the metabolism of dietary carcinogens or anti-carcinogens. A study of 500 incident colorectal cancer cases and population controls, matched for age, sex and general practitioner, was conducted in the United Kingdom to investigate whether 6 such genes (CYP1A1, GSTT1, GSTM1, GSTP1, EPHX1 and NQO1) modify the relationship between diet and disease risk. Usual diet was estimated using a detailed questionnaire administered by interview. Fruit and vegetable consumption were both found to protect against colorectal cancer, while overall meat and red meat consumption were found to increase risk. There was some evidence of interaction between GSTT1 and vegetable consumption (p=0.006, not adjusted for multiple tests) but no evidence of interaction with GSTM1. The protective effect of vegetables was only seen in those with deficient or intermediate GSTT1 predicted phenotype [OR 0.3, 95% confidence interval (0.1, 0.6), and OR 0.6 (0.4, 0.96), OR 1.4 (0.3, 2.4) for those with fast phenotype], and a similar result was observed for cruciferous vegetables. There was also weak evidence of interaction between red meat intake and GSTT1 (p=0.06), GSTP1 (p=0.16, with p=0.02 after adjustment for potential confounders) and NQO1 predicted phenotype (p=0.01). Because of the multiple hypotheses tested in our study, these findings require independent confirmation. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:259 / 264
页数:6
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