Polymorphism in DNA repair genes and oral squamous cell carcinoma in Thailand

Kietthubthew, Suparp; Sriplung, Hutcha; Au, William W.; Ishida, Takafumi

doi:10.1016/j.ijheh.2005.06.002

Cited by 104 publications

(94 citation statements)

References 22 publications

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“…Other studies also reported both presence and absence of association between polymorphisms at XPD and risk of head and neck/oral cancer in different populations. 14,25,26 Distribution of (Table III) were observed to be similar to those (6, 37 and 57%, respectively) in Caucasian population 11 but different from those in South East Asians and Eskimos (10-30% and 5% slow acetylators, respectively). 7 None of the NAT2 genotypes and acetylation status was associated with increased risk of cancer or leukoplakia in overall population (Table III) although only a few studies on Japanese and Caucasian populations have shown increased risk of head and neck cancer in a subset of slow acetylators.…”

Section: Discussionmentioning

confidence: 62%

Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators

Majumder

Sikdar

Ghosh

et al. 2007

Intl Journal of Cancer

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Polymorphisms at N-acetyl transferase 2 locus (NAT2) lead to slow, intermediate and rapid acetylation properties of the enzyme. Improper acetylation of heterocyclic and aromatic amines, present in tobacco, might cause DNA adduct formation. Generally, DNA repair enzymes remove these adduct to escape malignancy. But, tobacco users carrying susceptible NAT2 and DNA repair loci might be at risk of oral leukoplakia and cancer. In this study, 389 controls, 224 leukoplakia and 310 cancer patients were genotyped at 5 polymorphic sites on NAT2 and 3 polymorphic sites on each of XRCC1 and XPD loci by PCR-RFLP method to determine the risk of the diseases. None of the SNPs on these loci independently could modify the risk of the diseases in overall population but variant genotype (Gln/Gln) at codon 399 on XRCC1 and major genotype (Lys/Lys) at codon 751 on XPD were associated with increased risk of leukoplakia and cancer among slow acetylators, respectively (OR 5 4.2, 95% CI 5 1.2-15.0; OR 5 1.6, 95% CI 5 1.1-2.3, respectively). Variant genotype (Asn/Asn) at codon 312 on XPD was also associated with increased risk of cancer among rapid and intermediate acetylators (OR 5 1.9, 95% CI 5 1.2-2.9). Variant C-G-A haplotype at XRCC1 was associated with increased risk of leukoplakia (OR 5 1.7, 95% CI 5 1.2-2.4) but leukoplakia and cancer in mixed tobacco users (OR 5 3.1, 95% CI 5 1.4-7.1, OR 5 2.4, 95% CI 5 1.1-5.4, respectively) among slow acetylators. Although none of the 3 loci could modulate the risk of the diseases independently but 2 loci in combination, working in 2 different biochemical pathways, could do so in these patient populations. ' 2007 Wiley-Liss, Inc.Key words: tobacco use; oral cancer; leukoplakia, NAT2; XPD; XRCC1; polymorphism As an early sign of damage to oral mucosa, tobacco smokers and chewers often develop different precancerous lesions, such as leukoplakia, erythroplakia, submucous fibrosis, etc., and these lesions are easily accessible to diagnosis. Annual incidence of oral leukoplakia has been reported as 0.2-11.7% in different populations of India 1-3 and about 2-12% of leukoplakia becomes malignant within several years. 2 Since leukoplakia is one of the good predictors of oral cancer so diagnosis and treatment of leukoplakia will be a useful strategy to control oral cancer incidence. Annually about 270,000 cases of oral cancer are reported worldwide but about 82,000 of them are diagnosed in India. 4 Major procarcinogens present in the tobacco smoke are polycyclic aromatic hydrocarbons, aromatic and heterocyclic amines and nitroso-compounds whereas nitrosamines and aromatic and heterocyclic amines are major components present in smokeless tobacco. Most of the tobacco carcinogens generally undergo bioactivation and inactivation by phase I and phase II enzymes respectively. Human N-acetylation transferase 2 (NAT2) is one of the phase II enzymes that participate in the bioconversion of aromatic and heterocyclic amines and variation in NAT2 enzyme activity is defined as polymorphism in N-acetylation capacit...

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Section: Discussionmentioning

confidence: 62%

Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators

Majumder

Sikdar

Ghosh

et al. 2007

Intl Journal of Cancer

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“…Through literature search and selection based on the inclusion criteria, 32 articles (37 studies) were found, and 28 articles (Bai et al 2007;Blankenburg et al 2005;Casson et al 2005;De Ruyck et al 2007;Festa et al 2005;Hansen et al 2007;Hirata et al 2007;Hu et al 2005;Huang et al 2006;Kietthubthew et al 2006;Lee et al 2005;Li et al 2006;Marin et al 2004;Mechanic et al 2006;Nelson et al 2005;Sak et al 2005Sak et al , 2006Sanyal et al 2004;Shen et al 2001Shen et al , 2005Sugimura et al 2006;Vogel et al 2005;Wang et al 2006;Weiss et al 2005;Yang et al 2005;Ye et al 2006;Zhou et al 2006;Zhu et al 2007) (32 studies) met our inclusion criteria, as listed in Table 1. One study of A33512C (Hirata et al 2006) reported an extremely high variant allele frequency, which may result from wrong allele counting or poor genotyping quality, and was finally excluded from our meta-analysis.…”

Section: Study Inclusionmentioning

confidence: 99%

“…Among the 28 eligible articles, 18 articles (Bai et al 2007;Blankenburg et al 2005;Festa et al 2005;Hansen et al 2007;Hirata et al 2007;Hu et al 2005;Huang et al 2006;Kietthubthew et al 2006;Lee et al 2005;Li et al 2006;Mechanic et al 2006;Sak et al 2005;Sanyal et al 2004;Vogel et al 2005;Weiss et al 2005;Ye et al 2006;Zhou et al 2006;Zhu et al 2007) (23 studies) described A33512C, ten articles (Bai et al 2007;Hu et al 2005;Huang et al 2006;Lee et al 2005;Li et al 2006;Sak et al 2006;Shen et al 2005;Weiss et al 2005;Zhou et al 2006;Zhu et al 2007) (11 studies) described C21151T, and 13 articles (Blankenburg et al 2005;Casson et al 2005;De Ruyck et al 2007;Kietthubthew et al 2006;Li et al 2006;Marin et al 2004;Nelson et al 2005;Sak et al 2005;Shen et al 2001;Sugimura et al 2006;Wang et al 2006;Yang et al 2005;Zhu et al 2007) (14 studies) described PAT -/+; 82.1% (23/28) stated that the age and gender status were matched between case and control popul...…”

Section: Study Inclusionmentioning

confidence: 99%

A meta-analysis of DNA repair gene XPC polymorphisms and cancer risk

Zhang

Chen

et al. 2007

J Hum Genet

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Polymorphisms (A33512C, C21151T and PAT -/+) of the xeroderma pigmentosum group C (XPC) were shown to contribute to genetic susceptibility to cancer. However, association studies on these polymorphisms in cancer have shown conflicting results. Thus, we performed a meta-analysis. Overall, there was no significant association between 33512C (9,091 patients and 11,553 controls) and cancer risk. No significant association was found in stratification analysis by tumor sites and ethnicities except an elevated lung cancer risk under the recessive genetic model in all subjects [P = 0.04, odds ratio (OR) = 1.20, 95% confidence interval (CI) 1.00-1.45, P heterogeneity = 0.88]. There was no significant association between 21151T (5,227 patients and 5,959 controls) and cancer risk in all subjects but an increased cancer risk in Caucasians under the recessive genetic model (P = 0.006, OR = 1.45, 95% CI 1.11-1.90, P heterogeneity = 0.75) and homozygote comparison (P = 0.02, OR = 1.41, 95% CI 1.07-1.81, P heterogeneity = 0.41). It might be that 21151T increases bladder cancer risk under the recessive genetic model (P = 0.02, OR = 1.49, 95% CI 1.06-2.09, P heterogeneity = 0.47) and homozygote comparison (P = 0.02, OR = 1.49, 95% CI 1.05-2.11, P heterogeneity = 0.23). There was no significant association between PAT + (4,600 patients and 4,866 controls) and cancer risk in all subjects. An increased cancer risk in Caucasians was found under the recessive genetic model (P = 0.02, OR = 1.20, 95% CI 1.03-1.40, P heterogeneity = 0.37) and homozygote comparison (P = 0.008, OR = 1.26, 95% CI 1.06-1.50, P heterogeneity = 0.13). The XPC PAT + allele might increase head and neck cancer risk (P = 0.02, OR = 1.29, 95% CI 1.04-1.59, P heterogeneity = 0.15). More studies based on larger, stratified, case-control population, especially studies investigate the combined effect of XPC A33512C, C21151T, and PAT, are required to further evaluate the role of these polymorphisms in different cancers.

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“…This change may influence their protein activity, resulting in differences of individual DNA repair capacity (DRC) that may affect the susceptibility of oral cancer. Growing number of studies have been done to examine the relationship between this SNP and the risks of oral cancer (Benhamou et al, 2004;Majumder et al, 2005;Matullo et al, 2006;Kietthubthew et al, 2006;Yang et al, 2008;Yen et al, 2008;Dos Reis et al, 2013). However, the results are inconclusive.…”

Section: Discussionmentioning

confidence: 99%

“…XRCC3 gene is involved in the repair of DNA double-strand breaks (DSB), which is important to prevent chromosomal fragmentation, translocations and deletions (Kanaar et al, 1998). To date, there are studies reporting the association between polymorphisms of XRCC3 codon 241 with oral cancer risk but these published data were contradictory (Benhamou et al, 2004;Majumder et al, 2005;Matullo et al, 2006;Kietthubthew et al, 2006;Yang et al, 2008;Yen et al, 2008;Dos Reis et al, 2013). Until now, there was no meta-analysis or systematic review on the risk of oral cancer with XRCC3 polymorphism.…”

Section: Introductionmentioning

confidence: 99%

Lack of Influence of an XRCC3 Gene Polymorphism on Oral Cancer Susceptibility: Meta-analysis

Zhang

Cui²,

Xu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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-1.11). In the stratified analysis by ethnicity, no significant associations were found among Asians and Caucasians. On stratification by tumor type, no significant associations were found for cancer and oral premalignant lesions. Conclusions: The XRCC3 gene polymorphism was not found to be associated with the risk of oral cancer. Considering the limited quality of the included case-control studies, more high quality studies with large sample size are needed to verify the above conclusion.

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Polymorphism in DNA repair genes and oral squamous cell carcinoma in Thailand

Cited by 104 publications

References 22 publications

Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators

Polymorphisms at XPD and XRCC1 DNA repair loci and increased risk of oral leukoplakia and cancer among NAT2 slow acetylators

A meta-analysis of DNA repair gene XPC polymorphisms and cancer risk

Lack of Influence of an XRCC3 Gene Polymorphism on Oral Cancer Susceptibility: Meta-analysis

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