Association of the GSTP1 and NQO1 Polymorphisms and Head and Neck Squamous Cell Carcinoma Risk

Cho, Chang Gun; Lee, Seok Ki; Nam, Soon-Yhul; Lee, Moo-Song; Lee, Sangwook; Choi, Eun Kyung; Park, Heon Joo; Kim, Sang Yoon

doi:10.3346/jkms.2006.21.6.1075

Cited by 29 publications

(19 citation statements)

References 20 publications

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“…The 105Val form shows altered affinity and enzymatic activity for some substrates. Four (18%) (77,(88)(89)(90) of the 22 studies (18,20,21,25,31,33,63,69,73,77,80,82,84,(87)(88)(89)(90)(91)(92)(93)(94) NATs. Two NAT isozymes, NAT1 and NAT2, are polymorphic and catalyze both O-acetylation (activation) and N-acetylation (usually detoxification) of aromatic and heterocyclic amine carcinogens.…”

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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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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“…In addition, the homozygous mutant (T/T) phenotype causes a complete lack of enzyme activity [3,5-7]. The NQO1 C609T polymorphism has been associated with the risk of various cancers such as renal [8], lung [9,10], esophageal [11-13], colorectal [14], and head and neck [15]. However, the results of some studies on the effect of the NQO1 C609T polymorphism on esophageal cancer are debatable.…”

Section: Introductionmentioning

confidence: 99%

NQO1 C609T polymorphism and esophageal cancer risk: a HuGE review and meta-analysis

Zhang

et al. 2013

BMC Med Genet

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BackgroundMany studies have been carried out to test the hypothesis that the NQO1 C609T polymorphism might be associated with the risk of esophageal cancer. However, the results are poorly consistent, partly due to genetic or other sources of heterogeneity. To investigate the association between this polymorphism and the risk of esophageal cancer, a meta-analysis was performed.MethodsWe used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of association. The frequency of the putative risk allele in the controls was estimated by the inverse-variance method. Cochran’s Q statistic and the inconsistency index (I2) were used to check heterogeneity. Egger’s test and an inverted funnel plot were used to assess the publication bias.ResultsOur study included eight published case-control studies about the NQO1 C609T polymorphism and esophageal cancer, including a total of 1,217 esophageal cancer patients and 1,560 controls. Overall, a significant association was found between the NQO1 C609T variant and esophageal cancer under a recessive model (OR = 1.647; 95% CI = 1.233-2.200). Regarding histological type, more significant evidence was found for esophageal squamous cell carcinoma (ESCC) (OR = 2.03; 95% CI = 1.29-3.19) than esophageal adenocarcinoma (EAC) (OR = 1.61; 95% CI = 1.01-2.56) under a recessive model.ConclusionsThe meta-analysis suggests that the NQO1 C609T polymorphism considerably increases the risk of esophageal cancer.

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“…In none of the studies, authors subdivided by smoking status in their analysis, this makes the comparison with the current study difficult. Several studies have examined the relationship between the NQO1 genetic polymorphisms and tobacco-related cancers, including lung, bladder, colorectal (Chao, Zhang, Berthiller, Boffetta, & Hashibe, 2006), esophageal Zhang, Schulz, et al, 2003), and head and neck (Cho et al, 2006), but the findings have been relatively inconsistent and varies across ethnic groups. A highquality meta-analysis of the NQO1 C609T polymorphism and risk of bladder, lung, and colorectal cancer revealed that there was significant heterogeneity across ethnic groups: The T allele was associated with an increased risk of bladder and colorectal cancer among whites, whereas a protective role was observed for the T allele among Asian populations (Chao et al, 2006).…”

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confidence: 99%