Glutathione S -transferase polymorphisms and risk of colorectal adenomas

Inoue, Hisako; Kiyohara, Chikako; Shinomiya, Sachiko; Marugame, Tomomi; Tsuji, Emiko; Handa, Koichi; Hayabuchi, Hitomi; Eguchi, Hironobu; Fukushima, Yoshitaka; Kono, Suminori

doi:10.1016/s0304-3835(00)00692-3

Cited by 15 publications

(14 citation statements)

References 20 publications

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“…[112][113][114][115] The lack of interaction between GSTT1 genotype and smoking is consistent with previous studies of colorectal cancer 103,104 and colorectal adenoma. 116,117 In contrast to Turner et al, 96 we did not observe an interaction between GSTT1 genotype and intake of green leafy vegetables. The lack of such interaction in our data, together with absence of interaction with smoking or with intake of meat, may in part reflect low statistical power to detect interaction, a problem that is also apparent in previous attempts to investigate interaction with smoking 101,103 and meat intake.…”

Section: Discussioncontrasting

confidence: 99%

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Little

Sharp

Masson

et al. 2006

Intl Journal of Cancer

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Cytochrome P-450 CYP1A1 is involved in the metabolism of polycyclic aromatic hydrocarbons (PAHs) that are derived from meat intake and tobacco smoking. Expression of the CYP1A1 gene is induced by compounds present in cruciferous vegetables. The glutathione S-transferases play a central role in the detoxification of carcinogens, including PAHs. We investigated the association between colorectal cancer and three variants (CYP1A1*2A, CYP1A1*2C, CYP1A1*4) of the CYP1A1 gene, and homozygosity for the null deletion of the GSTM1 and GSTT1 genes, and the joint effects of these genotypes and smoking, meat intake and intake of green leafy vegetables in a population-based study of 264 cases and 408 controls in Northeast Scotland. There was an inverse association with the CYP1A1*4 (m4) variant (OR 0.3, 95% CI 0.13-0.70). The OR for the CYP1A1*2C (m2) variant was 1.3 (95% CI 0.59-2.91), which is similar to a combined estimate for previous studies (OR 1.2, 95% CI 0.95-1.41). We observed no association with the CYP1A1*2A (m1) variant, or the GSTM1 and GSTT1 polymorphisms. Significant interactions between all 3 CYP1A1 variants and meat intake, and between the m1 and m2 variants and intake of green leafy vegetables, were observed. There was no evidence of interaction between CYP1A1 and smoking, and no evidence of interaction between the GSTM1 or GSTT1 polymorphisms and smoking, meat intake, green leafy vegetable intake, CYP1A1 variants or each other. ' 2006 Wiley-Liss, Inc.Key words: colorectal neoplasms; cytochrome P-450 CYP1A1; GSTM1 protein; glutathione S-transferase T1; polymorphism Evidence on the association between colorectal cancer and consumption of cooked meats, 1 tobacco smoking 2,3 and vegetable intake, 4-6 all of which are modifiable exposures with a potentially major public health impact, is inconsistent. Randomized trials 7,8 have confirmed evidence from most observational studies, [9][10][11][12] indicating an inverse relation between postmenopausal oestrogen replacement therapy and colorectal cancer, but considerable heterogeneity in the magnitude of this association was apparent. It is possible that these inconsistencies are in part due to differences between populations in the frequency of variants of genes, whose products modulate the effects of these exposures.A possible unifying factor underlying exposure to cooked meats, tobacco smoke and postmenopausal oestrogen replacement therapy is the presence of polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines. Cooking of meat and fish results in the formation of PAHs and, particularly at high temperatures, heterocyclic amines, which are carcinogenic in animals. [13][14][15] Tobacco smoking is another source of PAH exposure.16 PAHs affect oestrogen production and metabolism. 17CYP1A1 is expressed in the large bowel. 18,19 Because of the involvement of CYP1A1 in the metabolism of PAHs and oestrogens, and perhaps cruciferous vegetables and heterocyclic amines [20][21][22][23][24][25] (Table I), it might be expected that CYP1A1 variants might influence t...

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Section: Discussioncontrasting

confidence: 99%

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Little

Sharp

Masson

et al. 2006

Intl Journal of Cancer

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“…Among those papers, one paper was for colorectal cancer, and one study did not provide sufficient data [16,17]; therefore, they were excluded. The data of seven papers [10,14,[18][19][20][21][22] were overlapped, and four of them were excluded [10,18,19,21] according to the above statements. At last, 14 papers were included in this metaanalysis [4, 8, 9, 12-14, 20, 22-28].…”

Section: Eligible Studies Selectionmentioning

confidence: 99%

“…Eight papers for EPHX1 [4,[8][9][12][13]22,[27][28]; [2]. Five studies for GSTM1 [4,8,14,[24][25]; [3]. Four studies for GSTP1 [4,8,[24][25]; [4].…”

Section: After Removing Duplications Among the Databases 38 Papers Rmentioning

confidence: 99%

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System review and metaanalysis of the relationships between five metabolic gene polymorphisms and colorectal adenoma risk

et al. 2011

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The relationships between some metabolic (including EPHX1, GSTs and NQO1) gene polymorphisms and colorectal adenoma (CRA) risk have been commonly studied, and no conclusions are available up to now. Therefore, we quantitatively studied the relationships by a metaanalysis. The databases of Medline and Embase were retrieved updated to June 15th, 2011. Crude or adjusted odds ratio (crude OR or adjusted OR) and 95% confidence interval (95%CI) were calculated to present the strength of the associations. Overall, nine case-control studies for EPHX1 Tyr113His and His139Arg, five case-control studies for GSTM1, four studies for GSTP1 Ile105Val, two studies for GSTP1 Ala114Val, six studies for GSTT1 and four studies for NQO1 Pro187Ser were included in this metaanalysis. The results of combined analyses indicated that EPHX1 Tyr113His and His139Arg, GSTT1, GSTM1, GSTP1 Ile105Val and Ala114Val were not associated with CRA risk [crude OR (95%CI): 0.98 (0.90-1.07) and P ( z-test) = 0.65 for EPHX1 His carriers vs. Tyr/Tyr; 1.05 (0.97-1.15) and P ( z-test) = 0.21 for EPHX1 Arg carriers vs. His/His; 1.05 (0.92-1.20) and P ( z-test) = 0.47 for GSTT1 Null vs. Present; 1.01 (0.90-1.13) and P ( z-test) = 0.90 for GSTM1 Null vs. Present; 1.04 (0.92-1.17) and P ( z-test) = 0.56 for G carriers vs. AA for GSTP1 Ile105Val; 0.88 (0.70-1.11) and P ( z-test) = 0.28 for T carriers vs. CC for GSTP1 Ala114Val]. In contrast, Ser allele of NQO1 Ser187Pro might be a modest risk factor for CRA development [1.19 (1.06-1.33) and P ( z-test) = 0.003 for Ser carriers vs. Pro/Pro]. To get more precise evidences, adjusted ORs (95%CI) for EPHX1 Tyr113His, His139Arg, GSTP1 Ile105Val and NQO1 Ser187Pro were also calculated based on adjusted ORs (95%CIs) reported in primary studies. The results still indicated that EPHX1 Tyr113His, His139Arg and GSTP1 Ile105Val were not associated with CRA risk except for NQO1 Ser187Pro. When subgroup analyses were performed for population-based case-control studies or studies in HWE for EPHX1 Tyr113His and His139Arg, and NQO1 Ser187Pro polymorphisms, the results were persistent. Although with modest limitations and biases, this metaanalysis suggests that EPHX1 Tyr113His and His139Arg, GSTT1, GSTM1, GSTP1 Ile105Val and Ala114Val polymorphisms may be not risk factors for CRA development, while Ser allele of NQO1 Ser187 Pro may be a modest risk factor for CRA development, and may be used with other genetic markers for screening CRA in the future.

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“…(Tarawneh et al, 2009). Amass evidence shows susceptibility to cancer is mediated by alterations in the detoxifying capacity of genetically determined factors that play a role in cellular defense mechanism against endogenous and exogenous substances, many of which have carcinogenic potential (Deakin et al, 1996;Inoue et al, 2001). There is also considerable data on the role of oxidative stress in relation to colorectal cancer risk (Yoshida et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The GSTP1 Ile105Val Polymorphism is not Associated with Susceptibility to Colorectal Cancer

Khabaz

2012

Asian Pacific Journal of Cancer Prevention

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The glutathione S transferase (GST) family is a major part of cellular defense mechanisms against endogenous and exogenous substances, many of which have carcinogenic potential. Alteration in the expression level or structure of the glutathione-S-transferase (GST) enzymes may lead to inadequate detoxification of potential carcinogens and consequently contribute to cancer development. A member of the glutathione-S-transferase (GST) family, GSTP1, is an attractive candidate for involvement in susceptibility to carcinogen-associated colorectal cancer. An AgG transition in exon 5 resulting in an Ile105Val amino acid substitution has been identified which alters catalytic efficiency. The present study investigated the possible impact of Ile105Val GSTP1 polymorphism on susceptibility to colorectal cancer. in Jordan We examined 90 tissue samples previously diagnosed with colorectal carcinoma, and 56 non-cancerous colon tissues. DNA was extracted from paraffin embedded tissues and the status of the GSTP1 polymorphism was determined using a polymerase chain reaction restriction fragment length polymorphism (RFLP) method. No statistically significant differences were found between colorectal cancer cases and controls for the GSTP1 Ile/Ile, Ile/Val and Val/Val genotypes. The glutathione S-transferase polymorphism was not associated with risk in colorectal cancer cases in Jordan stratified by age, sex, site, grade or tumor stage. In conclusion, the GSTP1 Ile105Val polymorphism is unlikely to affect the risk of colorectal cancer.

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Glutathione S -transferase polymorphisms and risk of colorectal adenomas

Cited by 15 publications

References 20 publications

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

Colorectal cancer and genetic polymorphisms of CYP1A1, GSTM1 and GSTT1: A case‐control study in the Grampian region of Scotland

System review and metaanalysis of the relationships between five metabolic gene polymorphisms and colorectal adenoma risk

The GSTP1 Ile105Val Polymorphism is not Associated with Susceptibility to Colorectal Cancer

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