Glutathione-S-transferase polymorphisms and risk of squamous-cell carcinoma of the head and neck

Cheng, Lie; Sturgis, Erich M.; Eicher, Susan A.; Char, David; Spitz, Margaret R.; Wei, Qingyi

doi:10.1002/(sici)1097-0215(19990621)84:3<220::aid-ijc4>3.0.co;2-s

Cited by 97 publications

(55 citation statements)

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“…Absence of GSTM1-specific product indicated homozygosity for the null allele. The GSTT1 genotype was determined according to the method of Pemble et al (1994) (Cheng et al, 1999;Jahnke et al, 1996;Jourenkova et al, 1998;Khuri et al, 1997;Park et al, 1997;Trizna et al, 1995). In this study we found no association between GSTM1 nullizygosity and SCCHN.…”

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confidence: 39%

“…A null polymorphism exists for both these genes in the population with a frequency that varies widely between ethnic groups (from 3.6 to 23.1% for GSTT1 and from 40.0 to 62.2% for GSTM1) (Hamel et al,unpublished results). Recently, (Cheng et al, 1999) presented data in this journal that suggested a role for GSTT1 and GSTM1 nullizygosity in susceptibility to SCCHN. They found a significant association between the risk of SCCHN and the GSTT1 null genotype (OR ϭ 2.27,, the GSTM1 null genotype (OR ϭ 1.50,) and both null genotypes combined (OR ϭ 3.64, (Foulkes et al, 1996).…”

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confidence: 99%

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Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

Hamel¹,

Karimi²,

Hébert‐Blouin³

et al. 2000

Int. J. Cancer

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Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco Tobacco and alcohol are important contributing factors to the development of squamous cell carcinoma of the head and neck (SCCHN) (Blot et al., 1988;Vokes et al., 1993). However, recent case-control studies indicate that SCCHN is also associated with a family history of this cancer (Copper et al., 1995;Foulkes et al., 1995Foulkes et al., , 1996. In addition, second primary tumors, which are often a hallmark of inherited susceptibility to cancer, occur in up to 30% of patients with SCCHN (Day and Blot, 1992;Jones et al., 1995). A family history of SCCHN is more common for these cases than for single primary cases (Bongers et al., 1995;Foulkes et al., 1996) and it has been reported that non-smoking SCCHN patients are significantly more likely to be mutagen-sensitive than current smokers . It is, therefore, reasonable to suspect a role for inherited factors in determining predisposition to SCCHN. Since large pedigrees with numerous cases of SCCHN are uncommon (Foulkes et al., 1996), genetic susceptibility to SCCHN is likely to be conferred by cancer genes of low penetrance.We and others (Vineis et al., 1994;Foulkes et al., 1996) All cases and controls were genotyped for presence or absence of both the GSTT1 and GSTM1 genes. Genotyping of GSTM1 was performed on genomic DNA by PCR amplification as previously described using three primers that amplify the GSTM1 sequence and a second internal control sequence simultaneously (Zhong et al.,1993). Absence of GSTM1-specific product indicated homozygosity for the null allele. The GSTT1 genotype was determined according to the method of Pemble et al. (1994) modified to incorporate the simultaneous amplification of partial ␤-globin sequences to serve as an internal control . As in the case of GSTM1, the absence of a GSTT1-specific product was indicative of homozygosity for the null allele.We observed 70 GSTT1 positives and 9 GSTT1 nulls in cases, compared with 81 positives and 20 nulls in controls (OR ϭ 2.57, p ϭ 0.04

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confidence: 39%

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confidence: 99%

Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

Hamel¹,

Karimi²,

Hébert‐Blouin³

et al. 2000

Int. J. Cancer

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“…In contrast to the GST super family of enzymes that have been studied extensively for tobacco carcinogenesis (Nakajima et al, 1995;Cheng et al, 1999;Buch et al, 2002;Jhavar et al, 2004Jhavar et al, , 2005, other phase II metabolising enzymes such as the SULT have been less extensively studied (Hung et al, 2004;Dandara et al, 2006;Pachouri et al, 2006). There also has not been any collation of published data or a meta-analysis of case -control studies evaluating SULT enzyme in cancers.…”

Section: Discussionmentioning

confidence: 99%

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

et al. 2008

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Cytosolic sulphotransferase SULT1A1 plays a dual role in the activation of some carcinogens and inactivation of others. A functional polymorphism leading to Arg 213 His substitution (SULT1A1*2) affects its catalytic activity and thermostability. To study the association of SULT1A1*2 polymorphism with tobacco-related cancers (TRCs), a case -control study comprising 132 patients with multiple primary neoplasm (MPN) involving TRC and 198 cancer-free controls was carried out. One hundred and thirteen MPN patients had at least one cancer in upper aerodigestive tract including lung (UADT-MPN). SULT1A1*2 showed significant risk association with UADT-MPN (odds ratio (OR) ¼ 5.50, 95% confidence interval (CI): 1.09, 27.7). Meta-analysis was conducted combining the data with 34 published studies that included 11 962 cancer cases and 14 673 controls in diverse cancers. The SULT1A1*2 revealed contrasting risk association for UADT cancers (OR ¼ 1.62, 95% CI: 1.12, 2.34) and genitourinary cancers (OR ¼ 0.73, 95% CI: 0.58, 0.92). Furthermore, although SULT1A1*2 conferred significant increased risk of breast cancer to Asian women (OR ¼ 1.91, 95% CI: 1.08, 3.40), it did not confer increased risk to Caucasian women (OR ¼ 0.92, 95% CI: 0.71, 1.18). Thus risk for different cancers in distinct ethnic groups could be modulated by interaction between genetic variants and different endogenous and exogenous carcinogens.

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“…Sixteen (28%) (30,35,55,58,62,64,(66)(67)(68)71,72,74,79,(84)(85)(86) of the studies showed a significantly higher risk for HNC in subjects with the null Twenty-three (55%) ORs from 42 studies of the null GSTT1 genotype vs. the positive genotype were >1, and 7 studies (56,64,72,83,85,95,96) showed a significantly higher risk for HNC in subjects with the null genotype than in those with the positive genotype, suggesting that the null GSTT1 genotype may be associated with increased risk for HNC. In contrast, only 1 study showed a significantly lower risk with the null GSTT1 genotype than the positive genotype.…”

Section: Carcinogen Metabolic Genesmentioning

confidence: 99%

Genetic polymorphisms and head and neck cancer risk (Review)

Hiyama¹,

Yoshihara²,

Tanaka³

et al. 2008

Int J Oncol

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Abstract. The aim of this report is to review and evaluate, in a comprehensive manner, the published data regarding the contribution of genetic polymorphisms to risk of head and neck cancer (HNC). All relevant studies available in MEDLINE and published before July 2007 were identified. Studies carried out in humans that compared HNC patients with at least 1 standard control group were considered for analysis. Two hundred and eighteen publications and 3 published metaanalyses were identified. Seventy-five (34%) studies were conducted in Asian, 72 (33%) in American, and 68 (31%) in European countries. The most widely studied gene was GSTM1 (58 studies), followed by GSTT1 (42 studies), GSTP1 (codon 105, 22 studies) and p53 (codon 72, 20 studies). GSTM1, GSTT1, GSTP1, XRCC1 codons 194 and 399, and CYP1A1 codon 462 were examined by meta-analyses, and significant relations were found between the GSTM1-null genotype and an increased risk for HNC. In addition, increased risk for HNC was associated consistently with the ALDH2*1/*2, p53 codon 72 Pro/Pro and EPHX1 codon 113 Tyr/His and His/His genotypes. Cohort studies that simultaneously consider multiple genetic and environmental factors possibly involved in carcinogenesis of the head and neck are needed to ascertain not only the relative contribution of these factors to tumor development but also the contributions of their putative interactions. IntroductionHead and neck cancers (HNCs), including cancers of the oral cavity, pharynx and larynx, represent the 6 most frequent cancers and the seventh leading cause of cancer-related death worldwide. There are approximately 540,000 new cases and 271,000 deaths annually worldwide for a mortality of approximately 50% (1). HNCs represent approximately 3% of all cancers in the United States whereas these cancers are much more prevalent in other areas of the world, such as India, Thailand and Brazil (1,2). Standard therapeutic approaches, which focus on surgery, irradiation and chemotherapy (alone or in combination), have been modified over the last 30 years; however, the overall survival of HNC patients has not improved substantially. For patients affected by early-stage cancers with a high disease-specific survival rate, secondary tumors represent the most common cause of death (3). Furthermore, patients with advanced cancers have a high risk of primary treatment failure and death.Development of HNC is a multifactorial process associated with a variety of risk factors. Major risk factors in developed countries include smoking tobacco and drinking alcohol, and chewing betel quid (4,5). For tobacco smoking, a dose-response trend has been reported. Relative risks of developing laryngeal and oropharyngeal cancers are 1.8 and 1.3, respectively, for persons who smoke ≤30 cigarettes per day and 7.7 and 2.9, respectively, for persons who smoke >30 cigarettes per day compared with non-smokers (6). Alcohol consumption is also linked to increased risk of HNCs. For persons who consume >4 drinks (=47.5 g of pure ethanol) per day, the relati...

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Glutathione-S-transferase polymorphisms and risk of squamous-cell carcinoma of the head and neck

Cited by 97 publications

References 16 publications

Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

Increased risk of head and neck cancer in association with GSTT1 nullizygosity for individuals with low exposure to tobacco

Case–control study and meta-analysis of SULT1A1 Arg213His polymorphism for gene, ethnicity and environment interaction for cancer risk

Genetic polymorphisms and head and neck cancer risk (Review)

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