Abstract
The possible interplay between cruciferous vegetable consumption, functional genetic variations in glutathione S-transferases (GST) M1, T1, P1, and A1, and colorectal adenomas, was investigated in a Dutch case-control study. The GSTM1 and GSTT1 deletion polymorphisms, and the single nucleotide polymorphisms in GSTP1 (A313G) and in GSTA1 (C-69T) were assessed among 746 cases who developed colorectal adenomas and 698 endoscopy-based controls without any type of colorectal polyps. High and low cruciferous vegetable consumption was defined based on a median split in the control group. High consumption was slightly positively associated with colorectal adenomas [odds ratio (OR) 1.15; 95% confidence interval, 0.92-1.44]. For GSTP1, a positive association with higher cruciferous vegetable intake was only apparent in individuals with the low-activity GSTP1 genotype (GG genotype, OR 1.94; 95% confidence interval, 1.02-3.69). This interaction was more pronounced in men, with higher age and with higher meat intake. The GSTA1 polymorphism may have a modifying role as well: the OR for higher intake compared with lower intake was 1.57 (0.93-2.65) for individuals homozygous for the low expression variant (TT genotype). This seemed to be stronger with younger age and higher red meat intake. Cruciferous vegetable consumption and the combined GSTA1 and GSTP1 genotypes showed a statistically significant interaction (P = 0.034). The GSTM1 and GSTT1 genotypes did not seem to modify the association between cruciferous vegetable intake and colorectal adenomas. In conclusion, GSTP1 and GSTA1 genotypes might modulate the association between cruciferous vegetable intake and colorectal adenomas.
Highlights
Diet and other life-style factors are thought to play a major role in the colorectal neoplastic process [1, 2]
Sporadic colorectal cancers arise from acquired DNA alterations which progressively facilitate uncontrolled cell growth, are predominantly epithelial, and most are preceded by adenomas [3]
The involvement of glutathione S-transferases (GST) in isothiocyanate metabolism has led to the hypothesis that, through slower excretion of isothiocyanates from the body in individuals with genetic variants associated with lower GST capacity, isothiocyanates have more opportunity to exert their chemoprotective effects in these individuals [17]
Summary
Diet and other life-style factors are thought to play a major role in the colorectal neoplastic process [1, 2]. Sporadic colorectal cancers arise from acquired DNA alterations which progressively facilitate uncontrolled cell growth, are predominantly epithelial, and most are preceded by adenomas [3]. Consumption of vegetables of the family Cruciferae— in Western food patterns consisting mostly of the genus Brassica, including cabbage, cauliflower, Brussels sprouts, and broccoli—has been associated with a decreased risk of colorectal adenomas and cancer [4], not consistently [5,6,7,8,9,10]. The involvement of GSTs in isothiocyanate metabolism has led to the hypothesis that, through slower excretion of isothiocyanates from the body in individuals with genetic variants associated with lower GST capacity, isothiocyanates have more opportunity to exert their chemoprotective effects in these individuals [17]
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