Polymorphisms of the glutathione S‐transferase P1 gene and head and neck cancer susceptibility

Ophuis, Michael B. Oude; Roelofs, Hennie M.J.; Brandt, Piet A. van den; Peters, Wilbert H.M.; Manni, Johannes J.

doi:10.1002/hed.10182

Cited by 20 publications

(18 citation statements)

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“…Ophuis et al (19) found that HNSCC patients with the GSTP1 G allele containing genotypes (GA and GG) showed increased odds ratios for smoking compared with the wild type GSTP1 genotype. However, McWilliams et al (20) found no association between the GSTP1 genotypes and smoking status in HNSCC risk.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2006

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The GSTP1 and NQO1 have been reported to be associated with an increased risk for smoking related head and neck squamous cell carcinoma (HNSCC). The purpose of this study was to determine the effect of these metabolic gene polymorphisms on the risk of HNSCC. The study population included 294 histologically confirmed HNSCC cases and 333 controls without cancer. Genotyping analysis of the GSTP1 Ile105Val and NQO1 Trp139Arg genes was performed by polymerase chain reaction-based techniques on DNA prepared from peripheral blood. The Mantel-Haenszel χ2 test was used for statistical analysis. The allele frequencies of the GSTP1 and NQO1 polymorphisms were not statistically significant between cases and controls. In analyzing the association between smoking amounts and genetic polymorphisms, GSTP1 and NQO1 polymorphisms were associated with cigarette smoking amounts in cases. G allele containing genotypes in GSTP1 and T allele containing genotypes in NQO1 were associated with a tobacco dose-dependent increase in risk of HNSCC and these genotype distributions were statistically significant (p<0.05). We found that the GSTP1 105Val allele and NQO1 139Arg allele were associated with tobacco dose-dependent increase in risk of HNSCC. GSTP1 and NQO1 genotype polymorphisms may play an important role in the development of smoking related HNSCC.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2006

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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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“…In a Dutch population, Oude et al, [77] observed homozygous GSTP1 BB genotypes in 12.3% patients with HNSCC (out of 235) and 13.6% in healthy controls (out of 285). No statistical differences were found for the GSTP1 AA(Ile/Ile) and GSTP1 AB(Ile/Val) or GSTP1BB (Val/Val) genotypes, which confirmed that GSTP1 polymorphism is not associated with altered susceptibility to HNSCC [77]. Similarly, Reszka et al [78] found no statistically significant risk of HNSCC in patients carrying GSTP1 105Val alleles in a Polish study population (OR=0.97; CI=0.59-1.58) [78].…”

Section: Gstp1mentioning

confidence: 97%

“…The GSTP1 gene is positioned on chromosome 11 (11q13), and has the variant polymorphic genotypes GSTP1 AB (Ile/Val) and GSTP1 BB (Val/Val) along with the wild-type GSTP1 AA (Ile/Ile) [77]. The GST Pi polymorphism has a transition of adenine (A) to guanine (G) at nucleotide 313 in exon 5 and results in the substitution of isoleucine (Ile) to valine (Val) at position 104 in the amino acid sequence of the protein [61].…”

Section: Gstp1mentioning

confidence: 99%

“…Previously, several studies showed polymorphism of the GSTP1 105 Val homozygous allele may elevante the risk of HNSCC, and meta-analysis done by Hashibe et al [74] also revealed that GSTP1(Ile/Val) or (Val/Val) genotypes exhibit enhanced risk (OR=1.10, 95% CI=0.92-1.31) compared to positive genotypes [74]. In a Dutch population, Oude et al, [77] observed homozygous GSTP1 BB genotypes in 12.3% patients with HNSCC (out of 235) and 13.6% in healthy controls (out of 285). No statistical differences were found for the GSTP1 AA(Ile/Ile) and GSTP1 AB(Ile/Val) or GSTP1BB (Val/Val) genotypes, which confirmed that GSTP1 polymorphism is not associated with altered susceptibility to HNSCC [77].…”

Section: Gstp1mentioning

confidence: 99%

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Head and Neck Squamous Cell Carcinoma: Prognosis using molecular approach

Mazumder

Nath

et al. 2014

Open Life Sciences

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Head and neck squamous cell carcinoma (HNSCC) is the fifth most prevalent cancer worldwide. Apart from various known clinicopathogical factors, it is still a major concern as many genetic and epigenetic alterations bring about the possibility of this deadly disease. The aim of this review is to explore the possible role of DNA repair pathways and the polymorphic status of DNA repair genes (XPA, XPC, XPD, XRCC1 and XRCC3) in the onset of HNSCC, along with sequence variations in genes such as Glutathione S-transferases (GSTT1, M1 and P1) that are significantly associated with HNSCC risk. We also focus on the p53 gene mutation induced by various etiological agents and threat factors with its implications towards HNSCC, and emphasise the current therapeutic interventions in treating HNSCC.

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Polymorphisms of the glutathione S‐transferase P1 gene and head and neck cancer susceptibility

Cited by 20 publications

References 30 publications

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

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

Genetic polymorphisms and head and neck cancer risk (Review)

Head and Neck Squamous Cell Carcinoma: Prognosis using molecular approach

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