Metabolic Polymoryphisms, Smoking, and Oral Cancer in Puerto Rico

Xie, Heng; Hou, Lifang; Shields, Peter G.; Winn, Deborah M.; Gridley, Gloria; Bravo-Otero, Eleuterio; Diehl, Scott R.; Bowman, Elise D.; Brown, Linda Morris; Hayes, Richard B.

doi:10.3727/096504003773994851

Cited by 26 publications

(26 citation statements)

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“…Of the 30 studies included in the meta-analysis, 17 were carried out in Asian countries, 73,74,77,78,80,84,86 -96 seven in American countries, 71,72,79,83,85,97,98 and six in Europe. 5,44,81,82,99,100 Hospital patients were used as controls in 16 studies.…”

Section: Resultsmentioning

confidence: 99%

“…The frequencies in India varied from 24% to 37%, 78,80,84,90,96 in Japan from 39.8% to 48.7% 73,77,[91][92][93][94] , although the only study from Taiwan observed a frequency of 57.7%. 95 In South America these values ranged from 38.2% to 48.7% 71,79,97,98 and in Europe and United States from 51% to 54.8%. 5,44,[81][82][83]99,100 For the CYP1A1 exon 7 polymorphism, large geographical heterogeneity could be observed.…”

Section: Population Frequenciesmentioning

confidence: 99%

“…Of the 30 studies in the meta-analysis, data for 14 studies were obtained for GSTM1 and/or CYP1A1. 5,44,71,72,[77][78][79][80][81][82][83][84][85][86] However, two of these studies reported CYP1A1 and GSTM1 data separately for the same subjects and were counted as a single study. 71,72 Among these 13 published studies, three provided unpublished data for CYP1A1 polymorphisms for the same subjects.…”

Section: Data Collectionmentioning

confidence: 99%

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Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Varela-Lema

Taioli

Ruano-Raviña

et al. 2008

Genetics in Medicine

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The association of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers was assessed through a metaanalysis of published case-control studies and a pooled analysis of both published and unpublished case-control studies from the Genetic Susceptibility to Environmental Carcinogens database (http://www.upci.upmc.edu/research/ccps/ccontrol/ index.html). Thirty publications used in the meta-analysis included a total of 7783 subjects (3177 cases and 4606 controls); 21 datasets, 9397 subjects (3130 cases and 6267 controls) were included in the pooled analysis. The GSTM1 deletion was 2-fold more likely to occur in African American and African cases than controls (odds ratio: 1.7, 95% confidence interval: 0.9-3.3), although this was not observed among whites (odds ratio: 1.0, 95% confidence interval: 0.9-1.1). The metaanalysis and pooled analysis showed a significant association between oral and pharyngeal cancer and the CYP1A1 MspI homozygous variant (meta-OR m2/m2 : 1.9, 95% confidence interval: 1.4-2.7; Pooled OR m2m2 : 2.0, 95% confidence interval:1.3-3.1; OR m1m2 or [infi]m2m2 : 1.3, 95% confidence interval: 1.1-1.6). The association was present for the CYP1A1 (exon 7) polymorphism (OR Val/Val : 2.2, 95% confidence interval: 1.1-4.5) in ever smokers. A joint effect was observed for GSTM1 homozygous deletion and the CYP1A1 m1m2 variant on cancer risk. Our findings suggest that tobacco use and genetic factors play a significant role in oral and pharyngeal cancer. Genet Med 2008:10(6):369-384. Key Words: GSTM1, CYP1A1, oral and pharyngeal cancers, epidemiology, meta-analysis and pooled analysis Glutathione S-transferasesThe Glutathione S-transferases (GSTs) comprise a family of phase II detoxifying enzymes that catalyze a large number of reactions taking place between the cytosolic glutathione and compounds containing an electrophilic center. 1 These enzymes are involved in the elimination of xenobiotics and endogenous products of oxidative stress formed as a result of aerobic metabolism, exposure to ionizing radiation or any other process that causes cellular damage. Substrates for GSTs include acetaldehyde and several polyaromatic hydrocarbons (PAHs) found in tobacco smoke. The main steps for GST catalysis includes the formation of a complex with the cytosolic glutathione and the ionization of the sulfydryl group of this enzyme bound to glutathione to yield a highly reactive thiolate anion through hydrogen bonding with the adjacent hydroxyl

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Section: Resultsmentioning

confidence: 99%

Section: Population Frequenciesmentioning

confidence: 99%

Section: Data Collectionmentioning

confidence: 99%

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Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Varela-Lema

Taioli

Ruano-Raviña

et al. 2008

Genetics in Medicine

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“…We identified 15 studies (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) with data regarding the relation of the CYP1A1 Ile-Val substitution at codon 462 to HNC. In 4 studies (14,19,22,24), the risk for HNC in subjects with the Ile/Val and/or Val/Val genotypes was significantly higher than that for subjects with the Ile/Ile genotype, suggesting that the Val allele may be associated with increased risk for HNC.…”

Section: Introductionmentioning

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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“…Some studies had demonstrated that smoking and alcohol consumption were two risk factors of oral cancer (Katoh et al, 1999;Xie et al, 2004;Sugimura et al, 2006;Cha et al, 2007;Halawany et al, 2013;Menezes et al, 2013). However, other studies were focus on genetic polymorphisms.…”

Section: Introductionmentioning

confidence: 99%

Null Glutathione S-transferase T1 and M1 Genotypes and Oral Cancer Susceptibility in China and India - a Meta-analysis

Peng

Liu²,

Zhu³

2014

Asian Pacific Journal of Cancer Prevention

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Objective: Genetic variation is considered to strongly impact on detoxification of carcinogens and therefore is related to cancer risk. However, findings for the null genotypes of GSTT1 and GSTM1 have not always been consistent. Therefore the present meta-analysis was conducted. Methods: We accessed the reported study at different research areas and used various databases, including PubMed and Wanfang Med Onlion from 1990 to May 1st 2013. We calculated the odds ratio (OR), 95% confidence interval (CI) and P value for oral cancer by using Review

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Metabolic Polymoryphisms, Smoking, and Oral Cancer in Puerto Rico

Cited by 26 publications

References 0 publications

Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Genetic polymorphisms and head and neck cancer risk (Review)

Null Glutathione S-transferase T1 and M1 Genotypes and Oral Cancer Susceptibility in China and India - a Meta-analysis

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