Gene–environment interaction involved in oral carcinogenesis: molecular epidemiological study for metabolic and DNA repair gene polymorphisms

Sugimura, Tomoko; Kumimoto, Hiroshi; Tohnai, Iwai; Fukui, Takafumi; Matsuo, Keitaro; Tsurusako, Shinichi; Mitsudo, Kenji; Tajima, Kazuo; Ishizaki, Kanji

doi:10.1111/j.1600-0714.2005.00364.x

Cited by 104 publications

(68 citation statements)

References 35 publications

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“…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%

“…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%

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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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Section: Study Inclusionmentioning

confidence: 99%

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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“…There has been increasing evidence that DNA damage plays a critical role in the carcinogenesis of most cancers and DNA En-Jiao Zhang 1 , Zhi-Gang Cui 2 , Zhong-Fei Xu 1 , Wei-Yi Duan 1 , Shao-Hui Huang 1 , Xue-Xin Tan 1 , Zhi-Hua Yin 3 , Chang-Fu Sun 1 , Li Lu 1 * repair genes are considered key genes associated with the onset of cancer (Berwick et al, 2000;Poirier, 2012;Jin et al, 2013). Some repair genes have been reported to be associated with oral cancer (Sugimura et al, 2006;Bau, 2012), including the X-ray repair cross complementing 3 (XRCC3) gene (Flores-Obando et al, 2010).…”

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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“…Thus far, several molecular epidemiological studies have investigated the association between the XPA A23G polymorphism and HNSCC risk (11)(12)(13)(14)(15)(16)(17)(18). However, the results remain inconsistent and controversial, partially due to the relatively small sample size of independent studies and sampling effects.…”

Section: Introductionmentioning

confidence: 99%

Association of the XPA A23G polymorphism with the risk of head and neck carcinomas: Evidence from 5,491 subjects

Gao

et al. 2015

Molecular and Clinical Oncology

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Abstract. The XPA gene participates in modulating DNA damage recognition during the DNA nucleotide excision repair process. Current data regarding the association of the XPA A23G polymorphism with the risk of head and neck squamous cell carcinoma (HNSCC) remain controversial, and meta-analyses focusing on the HNSCC risk and this polymorphism are limited. Therefore, the aim of the present study was to derive a more precise estimation of this association by a meta-analysis of all the eligible studies. Odds ratios (ORs) with 95% confidence intervals (CI) were assessed for the strength of the associations in eight studies, including 5,491 subjects (2,409 HNSCC cases and 3,082 controls). The overall analysis revealed that the XPA A23G polymorphism was not significantly associated with the overall HNSCC risk. Consistently, there was no evidence for the association between the XPA A23G polymorphism and HNSCC risk in subgroup analyses based on ethnicity and the source of controls. However, the significant associations in oral carcinoma with the increased risk among the XPA heterozygote (AG vs. AA: OR, 1.58; 95% CI, 1.06-2.37; P heterogeneity =0.23, I2 =30%) and dominant (AG +GG vs. AA: OR, 1.53; 95% CI, 1.04-2.23; P heterogeneity =0.21, I 2 =36%) models were observed in the subgroup analysis by tumor site. In conclusion, the meta-analysis suggested that the XPA A23G polymorphism was not associated with overall HNSCC susceptibility, but it was associated with oral carcinoma susceptibility and it may be a risk factor for oral carcinoma. Further well-designed and large studies are required to confirm these associations.

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Gene–environment interaction involved in oral carcinogenesis: molecular epidemiological study for metabolic and DNA repair gene polymorphisms

Abstract: CYP2E1, XPA and ERCC1 polymorphisms may affect the risk of OSCC.

Cited by 104 publications

References 35 publications

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

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

Association of the XPA A23G polymorphism with the risk of head and neck carcinomas: Evidence from 5,491 subjects

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