Head and Neck Squamous-Cell Cancer and its Association with Polymorphic Enzymes of Xenobiotic Metabolism and Repair

Harth, Volker; Schäfer, Martin; Abel, Josef; Maintz, Laura; Neuhaus, Thomas J.; Besuden, Mette; Primke, Robert; Wilkesmann, Anja; Thier, Ricarda; Vetter, Hans; Ko, Yon‐Dschun; Brüning, Thomas; Bolt, Hermann M.; Ickstadt, Katja

doi:10.1080/15287390801988160

Cited by 73 publications

(62 citation statements)

References 38 publications

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“…A total of 45 abstracts were retrieved through PubMed and Medline, and 2 additional articles were found through the ISI Web of Knowledge. After reviewing all 47 articles carefully, 16 eligible articles including 2,965 cases with HNC and 3,919 controls were identified and included in the final meta-analysis (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). The main characteristics of all 16 studies are described in Table I.…”

Section: Resultsmentioning

confidence: 99%

Association of NAT2 phenotype with risk of head and neck carcinoma: A meta-analysis

Zheng

Teng

et al. 2011

Oncology Letters

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Abstract. N-acetyltransferase 2 (NAT2) is a key enzyme involved in the metabolism of xenobiotics and plays a significant role in the detoxification of numerous potential carcinogens. According to its acetylation status, NAT2 acetylator may be classified into two phenotypes, rapid and slow. Numerous studies have demonstrated that the polymorphisms of NAT2 were correlated with individual susceptibility to several malignant neoplasms, including head and neck carcinomas (HNC). However, the associations between the acetylator phenotypes and HNC risk in each study were not entirely consistent. To assess these associations more comprehensively, we performed a meta-analysis. In this meta-analysis, 16 eligible studies including 2,965 cases with HNC and 3,919 controls were identified by searching the databases of PubMed, Medline and the ISI Web of Knowledge. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were used to evaluate the association. No significant associations between the rapid acetylator phenotype in NAT2 and HNC risk were found either in the overall analysis (OR=0.98; 95% CI 0.83, 1.15; I 2 =57%; P heterogeneity =0.003) or in the subgroup analysis by ethnicity (for the Caucasian population, OR=1.03, 95% CI 0.85, 1.24, I 2 = 63%, P heterogeneity = 0.002; for other mixed populations, OR=0.78, 95% CI=0.61, 1.00, I 2 = 0%, P heterogeneity =0.47). In conclusion, this meta-analysis suggested that there is no association between the NAT2 phenotype and the risk of HNC. IntroductionHead and neck carcinoma (HNC), arising from the sites of the oral cavity, oropharynx, hypopharynx and larynx, is the sixth most common type of cancer worldwide (1). It is characterized by a moderately low survival rate, a high recurrence rate, and a high rate of second primary malignancy (2). In 2009, approximately 49,260 new cases (35,530 males and 13,730 females) of HNC were diagnosed in the USA, and 11,480 deaths occurred (8,300 males and 3,180 females) (1). Present evidence has proven that numerous factors contribute to the risk of squamous cell carcinoma of the head and neck, including tobacco use, alcohol consumption (3), viral infection (4) and genetic polymorphisms (5). In particular, tobacco smoking and alcohol consumption account for approximately 80% of HNC cases (6,7). However, it is worth noting that only a fraction of smokers and alcohol consumers develop HNC. This phenomenon suggests that host factors, including genetic variation, contribute to the inter-individual variation in the susceptibility to HNC.Numerous procarcinogens are known to exist in tobacco, including polycyclic aromatic hydrocarbons (PAHs), aromatic and heterocyclic amines; nitroso-compounds in smoking tobacco; and nitrosamines, aromatic and heterocyclic amines in smokeless tobacco. Most of these carcinogens generally undergo bioactivation and inactivation by phase Ⅰ and Ⅱ enzymes, respectively. The phase Ⅱ enzymes, including Glutathione S-transferases (GSTs) and N-acetyltransferase (NAT), contribute to the detoxification metabolism. Human NAT compr...

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Section: Resultsmentioning

confidence: 99%

Association of NAT2 phenotype with risk of head and neck carcinoma: A meta-analysis

Zheng

Teng

et al. 2011

Oncology Letters

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“…They observed that carrying the XPD (Lys 751 Gln), Gln/Gln genotype was associated with HNSCC (OR=0.54; 95% CI = 0.35-0.92; P = 0.006) [44]. In another case-control study conducted by Harth et al [13] on 312 cases and 300 controls, the XPD (Lys 751 Gln) C/C genotype and combined XPD (Arg 156 Arg) C/A and A/A genotypes were predominant in HNSCC patients [13]. In a non-Hispanic white population, Sturgis et al [11] reported XPD (Lys 751 Gln, rs13181) gene polymorphism to have significant positive association with HNSCC risk [11].…”

Section: Nucleotide Excision Repair (Ner)mentioning

confidence: 99%

“…At the cellular and tissue level, these biological responses become modified by exogenous and endogenous compounds due to the occurrence of polymorphic alleles in DNA repair genes that alter the repair capacity, thereby developing different kinds of diseases, such as cancer [17]. The polymorphic DNA repair genes involved in HNSCC are grouped into four major DNA repair pathways: Base excision repair (BER), nucleotide excision repair (NER), double-strand DNA breaks repair (DSBR) and mismatch repair (MMR) [12][13][14].…”

Section: Genetic Polymorphisms With Impact On Dna Damage and Repairmentioning

confidence: 99%

“…Ironically, defects in these pathways have been implicated in causing excessive cell death or transformation of cells, resulting in increased risk of HNSCC [5,6]. Polymorphisms in DNA repair genes such as XPA (Xeroderma Pigmentosum Complementation group A) [7,8], XPC (Xeroderma Pigmentosum Complementation group C) [9,10], XPD (Xeroderma Pigmentosum Complementation group D) [11,12], XRCC1 (X-Ray Cross Complementing group 1) [13,14], XRCC3 (X-Ray Cross Complementing group 3) [15,16] and Phase II xenobiotic metabolizing genes such as Glutathione S-transferases (GSTs: M1, T1 and P1) have been reported in the pathophysiology of HNSCC [1,2,17]. Moreover, any catastrophic change in the p53 gene, along with poor diet and other occupational hazards, can bring about the occurrence of HNSCC [18].…”

Section: Introductionmentioning

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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“…Dentre elas destacam-se as CYP1A1 e CYP2E1. (Harth et al, 2008;Cury et al, 2012;Waters et al, 2010).…”

Section: Biomarcadores De Efeitounclassified

Avaliação citogenética e molecular de trabalhadores intoxicados pelo benzeno

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Head and Neck Squamous-Cell Cancer and its Association with Polymorphic Enzymes of Xenobiotic Metabolism and Repair

Cited by 73 publications

References 38 publications

Association of NAT2 phenotype with risk of head and neck carcinoma: A meta-analysis

Association of NAT2 phenotype with risk of head and neck carcinoma: A meta-analysis

Head and Neck Squamous Cell Carcinoma: Prognosis using molecular approach

Avaliação citogenética e molecular de trabalhadores intoxicados pelo benzeno

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