Single nucleotide polymorphisms of DNA repair genes XRCC1 and XPD and its molecular mapping in Indian oral cancer

Ramachandran, Surya; Ramadas, K; Hariharan, Ramkumar; Kumar, Raghu; Pillai, M. Radhakrishna

doi:10.1016/j.oraloncology.2005.08.010

Cited by 99 publications

(72 citation statements)

References 39 publications

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“…They showed that the XRCC1 Arg399Gln exhibited a risk of 3.9 (95% CI = 1.76-9.05) for smoking and 4.62 (95% CI = 1.24-17.2) for betel quid chewing. These results were consistent with the earlier report (Ramachandran et al 2006), which showed there was a modest positive association with smoking and betel quid users for subjects with XRCC1 399 codon variant genotypes. Two-fold increase in risk was associated with almost all genotypes studied (Ramachandran et al 2006).…”

Section: Discussionsupporting

confidence: 93%

“…These results were consistent with the earlier report (Ramachandran et al 2006), which showed there was a modest positive association with smoking and betel quid users for subjects with XRCC1 399 codon variant genotypes. Two-fold increase in risk was associated with almost all genotypes studied (Ramachandran et al 2006). As to the molecular mechanisms of tobacco carcinogens, polymorphisms at N-acetyl transferase 2 locus (NAT2) lead to rapid acetylation properties of the enzyme.…”

Section: Discussionsupporting

confidence: 93%

“…2) and cumulative analysis of all genotype studies, we conclude that bias is less likely to have occurred in the 8 phenotype studies. Two studies were the major sources of heterogeneity for the reason that, when studies 3 and 4 were excluded from the analysis, the heterogeneity was eliminated (Matullo et al 2006;Ramachandran et al 2006). Selection bias may be a major source of heterogeneity.…”

Section: Discussionmentioning

confidence: 99%

“…XRCC1 polymorphisms were first reported as a risk factor for oral cancer (Sturgis et al 1999). Since then, a number of studies have confirmed or refuted this phenomenon (Majumder et al 2005(Majumder et al , 2007Matullo et al 2006;Ramachandran et al 2006;Kietthubthew et al 2006;Ho et al 2007;Yen et al 2008). These disparate findings may be due to insufficient power in some studies, differences between cancer types, type of study populations and study design.…”

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confidence: 97%

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The Arg194Trp Polymorphism in the X-ray Repair Cross-Complementing Group 1 Gene as a Potential Risk Factor of Oral Cancer: A Meta-Analysis

Zhou

et al. 2009

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

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The Arg194Trp Polymorphism in the X-ray Repair Cross-Complementing Group 1 Gene as a Potential Risk Factor of Oral Cancer: A Meta-Analysis

Zhou

et al. 2009

Tohoku J. Exp. Med.

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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: 60%

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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Genetic polymorphisms in DNA base‐excision repair genes ADPRT, XRCC1, and APE1 and the risk of squamous cell carcinoma of the head and neck

Lü

et al. 2007

Cancer

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Objective Systemic sclerosis (SSc; scleroderma) is a systemic connective tissue disease with an extensive vascular component that includes aberrant microvasculature and impaired wound healing. The aim of this study was to investigate the presence of antiangiogenic factors in patients with SSc. Methods Plasma samples were obtained from 30 patients with SSc and from 10 control patients without SSc. The samples were analyzed for the ability of plasma to affect endothelial cell migration and vascular structure formation and for the presence of antiangiogenic activity. Results Exposure of normal human microvascular dermal endothelial cells to plasma from patients with SSc resulted in decreased cell migration (mean ± SEM 52 ± 5%) and tube formation (34 ± 6%) compared with that in plasma from control patients (P < 0.001 for both). SSc plasma contained 2.9‐fold more plasminogen kringle 1–3 fragments (angiostatin) than that in control plasma. The addition of angiostatin to control plasma resulted in inhibition of endothelial cell migration and proliferation similar to that observed in SSc plasma. In vitro studies demonstrated that granzyme B and other proteases contained in T cell granule content cleave plasminogen and plasmin into angiostatin fragments. Conclusion Plasminogen conformation in patients with SSc enables granzyme B and granule content protease to limit the proangiogenic effects of plasmin and increase the levels of antiangiogenic angiostatin. This increase in angiostatin production may account for some of the vascular defects observed in patients with SSc.

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Single nucleotide polymorphisms of DNA repair genes XRCC1 and XPD and its molecular mapping in Indian oral cancer

Cited by 99 publications

References 39 publications

The Arg194Trp Polymorphism in the X-ray Repair Cross-Complementing Group 1 Gene as a Potential Risk Factor of Oral Cancer: A Meta-Analysis

The Arg194Trp Polymorphism in the X-ray Repair Cross-Complementing Group 1 Gene as a Potential Risk Factor of Oral Cancer: A Meta-Analysis

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

Genetic polymorphisms in DNA base‐excision repair genes ADPRT, XRCC1, and APE1 and the risk of squamous cell carcinoma of the head and neck

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