Genetic polymorphisms in the tobacco smoke carcinogens detoxifying enzyme UGT1A7 and the risk of head and neck cancer

Lacko, Martin; Roelofs, Hennie M.J.; Morsche, R.H.M. te; Voogd, Adri C.; Ophuis, Michael B. Oude; Peters, Wilbert H.M.; Manni, Johannes J.

doi:10.1002/hed.21090

Cited by 42 publications

(54 citation statements)

References 21 publications

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“…Our results indicate that there was a significantly higher mEH expression in normal epithelium than those in bladder urothelial carcinoma (P<0.05) and there was lower mEH level in more higher histological grade, higher pT stage and more likely to relapse (P<0.05). These data were the same with previous reports about mEH was related with carcinoma (Kang et al, 2004;Nock et al, 2007;Hsu et al, 2008;Khedhaier et al, 2008;Lacko et al, 2009;Erkisi et al, 2010;Ihsan et al, 2010). These findings suggest the important role of mEH in bladder carcinogenesis, cancer development and recurrence, which support the effort to additionally investigate a mEH -based gene therapy.…”

Section: Discussionsupporting

confidence: 91%

Low Microsomal Epoxide Hydrolase Expression is Associated with Bladder Carcinogenesis and Recurrence

Zhang

Yu²,

Zhang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Microsomal epoxide hydrolase (mEH) plays a significant role in the metabolism of numerous xenobiotics and is associated with several forms of cancer. Here, we investigated the role of mEH expression in bladder carcinogenesis, subsequent progression and recurrence. The expression of mEH was analyzed by Western blot in 50 bladder urothelial carcinoma and 20 normal epithelial tissues. There was a significantly higher mEH expression in the normal epithelium (P<0.05) and mEH expression was lower in high stage than in low stage tumors (P<0.05). Further, immunohistochmistry in 106 bladder urothelial carcinoma demonstrated mEH expression to be negatively correlated with histological grade, pT stage and recurrence (P<0.05). These findings suggest the important role of mEH in bladder carcinogenesis, cancer development and recurrence, providing support for efforts to develop mEH-based gene therapy.

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Section: Discussionsupporting

confidence: 91%

Low Microsomal Epoxide Hydrolase Expression is Associated with Bladder Carcinogenesis and Recurrence

Zhang

Yu²,

Zhang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…This observation of null type mutation in GSTT1 might have susceptible status or protective role to the individual for various diseases related to tobacco or their respective drug substrates. GSTT1 null type mutation leading to susceptibility for various cancers and diseases among the high frequency populations, reported earlier by various investigators (Lacko et al, 2009;Mo et al, 2009;Sam et al, 2009;Chuang et al, 2011;Kumar et al, 2011) were not yet uniformly demonstrated. In our observation, the DNA adducts of tobacco were causing mutation in GSTT1 gene loci and nullifying its detrimental function in carcinogenic compound biotransformation ability.…”

Section: Discussionmentioning

confidence: 90%

“…KP Senthilkumar 1,2 , Ramasamy Thirumurugan 1,3 * survival factors and cause various cancers (Hecht, 1999;Lacko et al, 2009;Zhuo et al, 2009). Drug/Xenobiotic compound metabolizing enzymes are capable of regulating the removal of this exogenous and endogenous DNA adducts/carcinogens from the cell (Hecht, 2003;Lacko et al, 2009).…”

Section: Impact Of Tobacco On Glutathione S Transferase Gene Loci Of mentioning

confidence: 99%

“…Drug/Xenobiotic compound metabolizing enzymes are capable of regulating the removal of this exogenous and endogenous DNA adducts/carcinogens from the cell (Hecht, 2003;Lacko et al, 2009). The mutation observed in GSTM1 or T1 was a deletion mutation of null genotype and completely lost its functions to become susceptible to various cancers or diseases and further the inheritance of the same (Evans et al, 2004;Anantharaman et al, 2007;Mo et al, 2009;Sam et al, 2009;Amer et al, 2011;Chuang et al, 2011;Kumar et al, 2011).…”

Section: Impact Of Tobacco On Glutathione S Transferase Gene Loci Of mentioning

confidence: 99%

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Impact of Tobacco on Glutathione S Transferase Gene Loci of Indian Ethnics

Senthilkumar¹,

Ramasamy²

2012

Asian Pacific Journal of Cancer Prevention

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Background: Tobacco contains agents which generate various potent DNA adducts that can cause gene mutations. Production of DNA adducts may be neutralized by glutathione S transferase (GST) along with other phase I and phase II enzyme systems. The existence of null type of GST among the population increases the susceptibility to various disorders and diseases. The present study focuses on the impact of high tobacco usage and possible null type mutation in GST loci. Methods: Genotypes of GST were detected by multiplex polymerase chain reaction in unrelated 504 volunteers of high tobacco using natives of Gujarat. Allelic frequencies were calculated using Statistical Package for Social Studies-16 software. Hardy Weinberg Equilibrium (HWE) was calculated using Chi square test. Two sided Fisher's significance test was used to compare allelic frequencies of different populations. Results: The frequency of homozygous null genotype of GSTM1 and GSTT1 were 20% (95% CI 16.7-23.9) and 35.5% (95% CI 31.4-39.9) respectively. The GSTM1 and GSTT1 null allele frequency distribution in the Gujarat population was significantly deviating from HWE. GSTT1 null frequency of Gujaratians was significantly higher and different to all reported low tobacco using Indian ethnics, while GSTM1 was not differing significantly. Conclusion: Tobacco usage significantly influences the rate of mutation and frequency of GSTT1 and M1 null types among the habituates. The rate of mutation in GSTT1 loci was an undeviating response to the dose of tobacco usage among the population. This mutational impact of tobacco on GSTT1 postulates the possible gene -environment interaction and selection of null genotype among the subjects to prone them under susceptible status for various cancers and even worst to cure the population with GSTT1 dependent drugs.

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“…Cigarette smoke consists of 5000 chemicals, of which 60 compounds are carcinogenic, including nicotine, nitrosamines, polycyclic aromatic hydrocarbons (PAHs; e.g., benzo(a) pyrene), tobacco alkaloids (nornicotine, anatabine, anabasine), and benzene [107].…”

Section: Smoking Tobaccomentioning

confidence: 99%

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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Genetic polymorphisms in the tobacco smoke carcinogens detoxifying enzyme UGT1A7 and the risk of head and neck cancer

Abstract: Predicted high activity UGT1A7 polymorphisms were significantly associated with an increased risk of head and neck cancer.

Cited by 42 publications

References 21 publications

Low Microsomal Epoxide Hydrolase Expression is Associated with Bladder Carcinogenesis and Recurrence

Low Microsomal Epoxide Hydrolase Expression is Associated with Bladder Carcinogenesis and Recurrence

Impact of Tobacco on Glutathione S Transferase Gene Loci of Indian Ethnics

Head and Neck Squamous Cell Carcinoma: Prognosis using molecular approach

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