Detoxification of electrophilic compounds by glutathione S‐transferase catalysis: Determinants of individual response to chemical carcinogens and chemotherapeutic drugs?

Coles, Brian; Kadlubar, Fred F.

doi:10.1002/biof.5520170112

Cited by 192 publications

(114 citation statements)

References 34 publications

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“…Similar negative results were also observed in both populationbased studies and hospital-based studies. These results provide evidence to support the data reported by Coles et al who found that GST polymorphism was not a powerful predictor of tissue-specific GST expression (Coles and Kadlubar, 2003). Taken together, we may conclude that GSTM1 and GSTT1 homozygous deletion polymorphisms may not relate to the development of brain tumors.…”

Section: Discussionsupporting

confidence: 91%

Lack of Association Between GSTM1 and GSTT1 Polymorphisms and Brain Tumour Risk

Sima

Zhong²,

Liu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objective: Glutathione S-transferases (GSTs) are important enzymes that are involved in detoxification of environmental carcinogens. Molecular epidemiological studies have been conducted to investigate the association between GSTM1 and GSTT1 homozygous deletion polymorphisms and brain tumours but results have been conflicting. The aim of this study was to clarify this problem using a meta-analysis. Methods: A total of 9 records were identified by searching the PubMed and Embase databases. Fixed-and random-effects models were performed to estimate the pooled odds ratios. Results: No significant association was found between the GSTM1 and GSTT1 homozygous deletion polymorphisms and risk of brain tumours, including glioma and meningioma. Similar negative results were also observed in both population-based and hospital-based studies. Conclusion: These findings indicate that the GSTM1 and GSTT1 polymorphisms may not be related to the development of brain tumours.

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Section: Discussionsupporting

confidence: 91%

Lack of Association Between GSTM1 and GSTT1 Polymorphisms and Brain Tumour Risk

Sima

Zhong²,

Liu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…55 GSTP1 belongs to a family of phase II metabolic enzymes that has been shown to play a crucial role in detoxification and drugs cytotoxication by conjugating them with glutathione. 59 Moreover, our present report showed a significantly high hypermethylation rates (MI) in SV40-positive DLBCL cases compared with SV40-negative cases. Therefore, the significant association of promoter hypermethylation of several TSGs with the presence of SV40 DNA in DLBCLs supports a functional effect of the virus in those lymphomas.…”

Section: Discussionsupporting

confidence: 49%

Presence of simian virus 40 DNA sequences in diffuse large B‐cell lymphomas in Tunisia correlates with aberrant promoter hypermethylation of multiple tumor suppressor genes

Amara

Trimèche

Ziadi

et al. 2007

Intl Journal of Cancer

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The simian virus SV40 (SV40), a potent DNA oncogenic polyomavirus, has been detected in several human tumors including lymphomas, mainly in diffuse large B-cell type (DLBCL). However, a causative role for this virus has not been convincingly established. Hypermethylation in promoter regions is a frequent process of silencing tumor suppressor genes (TSGs) in cancers, which may be induced by oncogenic viruses. In this study, we investigated the relationship between the presence of SV40 DNA sequences and the methylation status of 13 TSGs in 108 DLBCLs and 60 nontumoral samples from Tunisia. SV40 DNA presence was investigated by PCR assays targeting the large T-antigen, the regulatory and the VP1 regions. Hypermethylation was carried out by methylationspecific PCR. SV40 DNA was detected in 63/108 (56%) of DLBCL and in 4/60 (6%) of nontumoral samples. Hypermethylation frequencies for the tested TSGs were 74% for DAPK, 70% for CDH1, SHP1, and GSTP1, 58% for p16, 54% for APC, 50% for p14, 39% for p15, 19% for RB1, 15% for BLU, 3% for p53, and 0% for p300 and MGMT. No hypermethylation was observed in nontumoral samples. Hypermethylation of SHP1, DAPK, CDH1, GSTP1 and p16 genes were significantly higher in SV40-positive than in SV40-negative DLBCL samples (p values ranging from 0.0006 to <0.0001). Our findings showed a high prevalence of SV40 DNA in DLBCLs in Tunisia. The significant association of promoter hypermethylation of multiple TSGs with the presence of SV40 DNA in DLBCLs supports a functional effect of the virus in those lymphomas. ' 2007 Wiley-Liss, Inc.Key words: diffuse large B-cell lymphomas; simian virus 40; hypermethylation; tumor suppressor genes; Tunisia Simian virus 40 (SV40) is a potent DNA oncogenic polyomavirus of rhesus monkey origin which seems to have spread to human beings via contamination of poliovirus stocks between 1955 and 1963 as well as by other means, 1 and mounting evidence suggests that it is an emergent human pathogen. 2-4 SV40 DNA sequences have been detected in pediatric and adult brain tumors, 5,6 mesotheliomas, 7 osteosarcomas, 8 bronchopulmonary carcinomas, 9 bone tumors 10 and papillary thyroid carcinomas. 11 There also increasing evidence that SV40 is associated with non-Hodgkin's lymphomas, particularly with diffuse large B-cell lymphomas (DLBCL), 12-21 in spite of several negative studies. [22][23][24] However, although these observations indicate an association between this virus and specific human tumors, they do not demonstrate a causal role, and the molecular mechanism by which SV40 thought to be involved is still unclear.SV40 oncogenic potential is assumed to be associated with the primary viral gene product, large T-antigen (Tag), protein responsible for SV40 replication and SV40-mediated cell transformation. 1 In vitro, the infection of human cells by SV40 has showed that SV40 Tag can promote malignancy transformation by blocking the products of several tumor suppressor genes (TSGs), 1,25 inducing telomerase activity, 26 and stimulating other oncogenes and growth facto...

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“…Genetic polymorphisms that affect the activity of GST enzymes have been identified in humans. Null variants of the GSTM1 gene and GSTT1 gene contain large deletions, and individuals who are homozygous for the GSTM1-null or GSTT1-null gene cannot produce the corresponding GST enzyme [60]. Lower GST activity in such individuals could result in slower elimination and longer exposure to isothiocyanates after cruciferous vegetable consumption [61].…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis

Higdon

Delage

Williams

et al. 2007

Pharmacological Research

917

697

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Cruciferous vegetables are a rich source of glucosinolates and their hydrolysis products, including indoles and isothiocyanates, and high intake of cruciferous vegetables has been associated with lower risk of lung and colorectal cancer in some epidemiological studies. Glucosinolate hydrolysis products alter the metabolism or activity of sex hormones in ways that could inhibit the development of hormone-sensitive cancers, but evidence of an inverse association between cruciferous vegetable intake and breast or prostate cancer in humans is limited and inconsistent. Organizations such as the National Cancer Institute recommend the consumption of 5-9 servings of fruits and vegetables daily, but separate recommendations for cruciferous vegetables have not been established. Isothiocyanates and indoles derived from the hydrolysis of glucosinolates, such as sulforaphane and indole-3-carbinol (I3C), have been implicated in a variety of anticarcinogenic mechanisms, but deleterious effects also have been reported in some experimental protocols, including tumor promotion over prolonged periods of exposure. Epidemiological studies indicate that human exposure to isothiocyanates and indoles through cruciferous vegetable consumption may decrease cancer risk, but the protective effects may be influenced by individual genetic variation (polymorphisms) in the metabolism and elimination of isothiocyanates from the body. Cooking procedures also affect the bioavailability and intake of glucosinolates and their derivatives. Supplementation with I3C or the related dimer 3,3′-diindolylmethane (DIM) alters urinary estrogen metabolite profiles in women, but the effects of I3C and DIM on breast cancer risk are not known. Small preliminary trials in humans suggest that I3C supplementation may be beneficial in treating conditions related to human papilloma virus infection, such as cervical intraepithelial neoplasia and recurrent respiratory papillomatosis, but larger randomized controlled trials are needed.

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Detoxification of electrophilic compounds by glutathione S‐transferase catalysis: Determinants of individual response to chemical carcinogens and chemotherapeutic drugs?

Cited by 192 publications

References 34 publications

Lack of Association Between GSTM1 and GSTT1 Polymorphisms and Brain Tumour Risk

Lack of Association Between GSTM1 and GSTT1 Polymorphisms and Brain Tumour Risk

Presence of simian virus 40 DNA sequences in diffuse large B‐cell lymphomas in Tunisia correlates with aberrant promoter hypermethylation of multiple tumor suppressor genes

Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis

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