CYP1A1 MspI polymorphism and the risk of oral squamous cell carcinoma: Evidence from a meta‑analysis

  • Authors:
    • Shang Xie
    • Chongdai Luo
    • Xiaofeng Shan
    • Shushan Zhao
    • Jing He
    • Zhigang Cai
  • View Affiliations

  • Published online on: February 5, 2016     https://doi.org/10.3892/mco.2016.768
  • Pages: 660-666
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Numerous case‑control studies have investigated whether the CYP1A1 gene polymorphism is involved in the occurrence of oral squamous cell carcinoma (OSCC); however, the conclusions are inconsistent. In order to further explore the correlation and obtain a strong conclusion, a meta‑analysis was performed to systematically assess the association between the CYP1A1 MspI polymorphism and risk of OSCC. In the present meta‑analysis, the odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were used to assess the association. The statistical analyses were performed with STATA 11.0 software. The heterogeneity was assessed by Q test and I2 test. The final analysis included 10 studies of 1,505 cases and 1,967 controls. The overall results suggested that the CYP1A1 MspI polymorphism was significantly associated with an increased risk of OSCC (CC+TC vs. TT: OR, 1.31; 95% CI, 1.01‑1.70; P=0.043; CC vs. TC+TT: OR, 2.38; 95% CI, 1.58‑3.58; P<0.001; CC vs. TT: OR, 2.52; 95% CI, 1.60‑3.96; P<0.001; and C vs. T: OR, 1.45; 95% CI, 1.15‑1.83; P<0.001). In a stratified analysis by ethnicity, a statistically significant correlation existed in the Asian population, but not mixed‑race and Caucasian populations. In conclusion, despite several limitations, the present meta‑analysis established that the CYP1A1 MspI polymorphism may be a risk factor for OSCC, particularly among the Asian population.

Introduction

Oral cancer is one of the most common cancers in the world and causes a considerable problem to global public health due to high mortality rates and disfigurement (1,2). Approximately 90% of malignant oral neoplasms are oral squamous cell carcinomas (OSCC), followed by adenocarcinoma and, rarely, other types (3). Despite advances in treatment for OSCC, the 5-year survival rate remains poor (46). Therefore, investigating the risk factors and developing the early diagnosis for treatment and prevention of OSCC are urgently required.

Epidemiological studies have shown that OSCC is associated with high tobacco use and alcohol consumption (79). However, not all individuals with tobacco and alcohol habits develop these fatal diseases, suggesting that individual genetic factors may also be involved in disease etiology. The research results of the human genome project have demonstrated that 99.9% of the genomes are the same between individuals, with little difference in single nucleotide polymorphisms (SNPs). Therefore, interindividual differences in expression of SNPs may contribute to the variability in the risk towards various types of malignancies, including OSCC. Currently, the published evidence shows that there were significant associations of gene polymorphisms with the susceptibility of numerous cancers, such as GST and CYP1A1 gene polymorphisms with squamous cell carcinoma of the lungs and head and neck cancer, and the 8q24 rsl3281615 polymorphism with the risk of breast cancer (1015). However, the associations of OSCC with CYP1A1 MspI genetic variants are inconsistent (1625).

Cytochrome P4501A1 (CYP1A1) is a member of the CYP family that participates in the metabolism of xenobiotics and endogenous compounds, encoding for the aryl hydrocarbon hydrolase, which is involved in the activation of polycyclic aromatic hydrocarbon (PAHs) and aromatic amines, and is expressed in oral tissue (26). CYP1A1 is able to activate carcinogenic PAHs and its expression and function are affected by gene polymorphisms, with more attention focused on the association of cancer and CYP1A1. According to the previous studies, the CYP1A1 gene has several SNPs that may alter the activities of their enzymes and increase carcinogen activation and yield to carcinogenicity. The first allele variants of the CYP1A1 gene (CYP1A1*2A or CYP1A1 MspI) are the most common polymorphisms, which are a transition from T to C in the 3′ non-coding region resulting in the introduction of an MspI restriction site and association with an increase in enzyme activity, thus affecting the risks of carcinoma (27,28). The MspI restriction site polymorphism results in three genotypes; wild-type (TT), heterozygous variant (TC) and homozygous variant (CC) (29).

Considering the significance of the CYP1A1 MspI polymorphism in the occurrence and development of malignancies, including OSCC, the role of the CYP1A1 MspI polymorphism in OSCC patients was systematically evaluated through a meta-analysis.

Materials and methods

Search strategy

Pubmed, Web of Science, China National Knowledge Infrastructure (CNKI) and WANFANG databases were searched without language limitations, and the last search was updated on May 3, 2014. The CNKI and WANFANG databases provided studies in Chinese and English. The search process was designed to primarily identify all the relevant studies and the search strategies are as follows: (CytochromeP450 1A1 or P4501A1 or CYP1A1 or CYP1A1*2A or MspI or T3801C), (genotype or polymorphism or allele or variant) and (oral squamous cell carcinoma or OSCC or mouth neoplasm or oral cancer or oral carcinoma or oral tumor). The results were screened by two investigators according to the title, key words, abstract and type of study, and irrelevant studies were removed. A manual review of the references cited in the selected studies was undertaken to retrieve studies that may have been missed in the search. Subsequently, the relevant studies were downloaded and further screened to identify the potentially eligible studies. When essential data were not provided in the original studies, every effort was made to contact the authors for confirmation.

Inclusion/exclusion criteria

All the relevant case-control studies were included, irrespective of languages. In the meta-analysis, the following criteria were set and reviewed by two independent investigators: i) Studies should be concerned with the association of the CYP1A1 MspI polymorphism with oral squamous cell carcinoma risk, and OSCC cases were histologically confirmed; ii) each trial should be an observational study (case-control or cohort) of human subjects; iii) studies must offer the size of the sample, and the genetic distribution or the original information that can help infer the results; and iv) when multiple studies from a particular research group reported data from overlapping samples, the study reporting the largest dataset was included.

Exclusion criteria included: i) Review studies, editorials or meta-analysis; ii) case reports or lack of case-control study; and iii) studies that estimated the risk of secondary tumors, recurrence or response to treatment. For a conflicting evaluation, an agreement was reached following a discussion. When a consensus could not be attained, another investigator was invited to resolve the dispute and a final result was generated by the majority. All the studies were viewed in accordance with the criteria defined above for further analysis.

Data extraction

All the data were independently reviewed and extracted with a standardized data-collection form by two investigators (Shang Xie and Chongdai Luo). Differences between the investigators were solved by discussion and when necessary, through consultation. The following characteristics were collected from each study: Ethnicity, country, sample size, control source, matching contents, Hardy-Weinberg equilibrium and the gene distribution of cases and controls. When the data were not clear or presented by the author in the publication, contact for further details was attempted.

Quality assessment

The Newcastle-Ottawa scale (NOS) quality evaluation criteria was performed to evaluate the methodological quality of the included studies and those with poor quality were excluded (30,31). The NOS system categorizes into three dimensions, which are selection, comparability and exposure (case-control studies), and the three dimensions included eight items. A star system was used to assess the quality of all the included studies. The NOS ranges from zero (the lowest) to nine (the highest) stars. The assessment was performed independently by two investigators and the discrepancy was resolved by a discussion.

Statistical analysis

All the data management and analysis for the meta-analysis was performed with STATA 11.0 software (Stata Corporation, College Station, TX, USA). The odds ratio (ORs) with corresponding 95% confidence intervals (CIs) were used to estimate the associations between the CYP1A1 MspI polymorphism and OSCC risks. In order to calculate the heterogeneity of the studies, the χ2 test was used and P<0.05 was considered to indicate a statistically significant difference (32). The inconsistency index, I2, was calculated to assess the variation caused by heterogeneity. When the P-value of the heterogeneity test was >0.10, the fixed-effects model was performed to calculate the combined OR, which assumed the same homogeneity of effect size across all the studies. When the P-value of the heterogeneity test was <0.10, the between-study heterogeneity was considered to indicate a statistically significant difference, and a random effect model was used to estimate the pooled OR. The funnel plot was used to test the underlying publication bias, and the funnel plot asymmetry was estimated by Egger's linear regression (33). Sensitivity analyses were performed to identify the influence of the individual studies on the combined OR. In the analysis, each study was excluded to assess whether stability between the remaining studies was reached.

Results

Characteristics of included studies

A total of 212 studies were retrieved by the literature search. In total, 171 studies were excluded as they were irrelevant to CYP1A1 MspI, OSCC or gene polymorphisms, and were not human studies. Two other potential eligible studies were obtained by screening the references of reviews. Following more detailed evaluations for the remaining 43 potential eligible studies, one study obtained from references did not meet the purpose of the meta-analysis (34), and four were reviews (26,3537). Following this, six studies only regarded CYP1A1 exon 7, but not CYP1A1 MspI (3843). Another sixteen studies were excluded as one of them presented overlapping data (44) and 15 failed to provide sufficient genotyping data (4559). In addition, there were five studies excluded as the cases were diagnosed as oral cancer only, and the identification of OSCC was not confirmed (6064). One study was excluded as the study only contained the cases and lacked the controls (65). Finally, 10 studies conformed to the inclusion criteria and were included in the meta-analysis of CYP1A1 MspI (1625). The search process is shown in Fig. 1.

A database with regard to the information extracted from each included study was established. Summaries of these studies are presented in Table I, which includes the first author, ethnicity, country, number and characteristics of cases and controls, and other necessary information. Of the 10 studies included in the meta-analysis, seven studies were performed in Asian countries, two in American countries and one in European countries. The number of cases and controls in the studies included varied from 38–446 and 81–727, respectively. The frequency of the CYP1A1 MspI homozygous variant allele (C/C) in the cases group varied from 0–30.0%, and 0–10.5% for the control group.

Table I.

Characteristics of the excluded studies evaluating the effects of the CYP1A1 MspI polymorphism on the susceptibility of OSCC.

Table I.

Characteristics of the excluded studies evaluating the effects of the CYP1A1 MspI polymorphism on the susceptibility of OSCC.

Cases, nControls, n


YearFirst author (ref)EthnicityQuality assessment (NOS)TTTCCCTTTCCCCases, nControls, nControl sourceMatchingHWE (control)
1999Sato (18)Asian8/9  56  5531  62  6515142142HealthyAge, gender0.738
1999Tanimoto (16)Asian8/9  32  5315  62  30  8100100HospitalAge, gender0.126
2002Kao (21)Asian6/9  40  5214  53  7914106146HospitalNA0.046
2003Gronau (22)Caucasian8/9  55  18  0100  35  1  73136HospitalAge, gender, tobacco and alcohol habits0.260
2006Gattás (23)Mixed-race8/9  25  13(TC+CC)  63  39(TC+CC)  38102HospitalAge, genderNA
2007Anantharaman (25)Asian8/92051954633134551446727Hospital, dental clinicAge, gender, tobacco habits0.002
2007Cha (24)Asian6/9  20  3022  49  9717  72163HospitalNA0.002
2008Losi-Guembarovski (20)Mixed-race7/9  55  27  9  53  23  5  91  81HospitalAge, gender, tobacco habits0.262
2008Sam (19)Asian8/9  77  8624115  9114187220HospitalAge, gender0.475
2012Shukla (17)Asian8/9  45  6045  72  72  6150150HospitalAge, gender, tobacco habits0.020

[i] NA, not available; HWE, Hardy-Weinberg equilibrium; NOS, Newcastle-Ottawa scale.

Results of quality assessment

According to the NOS system, all the included case-control studies were awarded a maximum of four stars in selection, two stars in comparability and three stars in exposure. The results of the assessment for the included studies ranged from six to eight stars (Table I), indicating that all the included studies were moderate-high qualities.

Test of heterogeneity and quantitative synthesis

A heterogeneity analysis was performed of the dominant (CC+TC vs. TT), recessive (CC vs. TC+TT) and additive models (CC vs. TT), and the results are shown in Table II. Owing to the overall heterogeneity observed in the dominant (CC+TC vs. TT: I2=64.4%, P=0.003), recessive (CC vs. TC+TT: I2=57.9%, P=0.015) and additive models (CC vs. TT: I2=61.0%, P=0.009), random-effect models were used to synthesize the data, respectively (Table II). The overall results suggested that the CYP1A1 gene variants (TC+CC or CC) have an increased risk of OSCC compared to those individuals with the positive homozygous carriers (TT). In order to further explore the observed heterogeneity, subgroup analyses were performed by ethnicity and 10 studies were divided into three subgroups: the Asian, Caucasian and mixed-race groups. However, the heterogeneity remained in the Asian population, but not in the mixed-race and Caucasian populations. For ethnicity, a significant increased risk was associated with the genetic variants among the Asian population, while no associations were found among the mixed ethnic and Caucasian populations (Fig. 2 and Table II).

Table II.

Main results of the heterogeneity test in the meta-analysis.

Table II.

Main results of the heterogeneity test in the meta-analysis.

CC+TC vs. TTCC vs. TC+TTCC vs. TT



CYP1A1 MspINo. of studies (case/controls)OR (95% CI)I2 (%) PQ-testP-valueOR (95% CI)I2 (%) PQ-testP-valueOR (95% CI)I2 (%) PQ-testP-value
Total ethnicity3372 (1405/1967)1.31 (1.01, 1.70)64.40.0030.0432.38 (1.58, 3.58)57.90.015<0.0012.52 (1.60, 3.98)61.00.009<0.001
Caucasian209 (73/136)0.91 (0.47, 1.75)0.775  0.62 (0.02, 15.39)   0.770  0.60 (0.02,15.07)   0.758
Asian2851 (1203/1648)1.43 (1.03, 1.99)74.30.0010.0322.52 (1.60, 3.98)67.00.006<0.0012.70 (1.63, 4.49)69.50.003<0.001
Mixed-race  312 (129/183)1.07 (0.66, 1.73)   0.00.4450.7981.67 (0.54, 5.20)   0.3781.73 (0.55, 5.51)   0.351

[i] OR, odds ratio; CI, confidence interval; I2, variation in OR attributable to heterogeneity; PQ-test >0.05, heterogeneity was not statistically significant; P>0.05, no statistical significance.

As for the C and T allele of CYP1A1 MspI, the results of the heterogeneity test and quantitative synthesis of C vs. T model, the pooled OR, 1.447; 95% CI, 1.146–1.827; I2=74.8%; PQ- test=0.000; and P<0.05 (Fig. 3) suggested that the C allele was significantly associated with an increased OSCC risk.

Publication bias analysis

The Begg's funnel plot was used to assess the possible publication bias. The Egger's linear regression is for the quantitative evaluation of the meta-analysis funnel plot symmetry and the results were as follows: i) CC+TC vs. TT model: Begg's test, P=0.858>0.05 and Egger's linear regression test: t=0.85, P=0.419>0.05; ii) CC vs. TC+TT model: Begg's test, P=0.711>0.05 and Egger's linear regression test: t=1.05, P=0.335>0.05; iii) CC vs. TT model: Begg's test, P=0.266>0.05 and Egger's linear regression test: t=1.20, P=0.276>0.05; and iv) C vs. T allele model: Begg's test, P=1.000>0.05 and Egger's linear regression test: t=0.99, P=0.354>0.05. The data of the four models indicated that the funnel plots were symmetrical for all.

Sensitivity analysis

In order to assess the stability of the results and reflect the influence of each study on the pooled ORs, sensitivity analysis was performed by excluding each case-control study individually. All the estimates were included between the lower and upper CI limits, suggesting the stability of the results in the meta-analysis.

Discussion

Oral cancer is cancer of the mouth, including squamous cell carcinoma, adenocarcinoma and verrucous carcinoma. Different histopathological types of cancers may have different genetic susceptibilities, such as CYP1A1 MspI polymorphism being a risk factor of squamous cell carcinoma of the lung, but varies in different histological types (13,66). Therefore, it is more reasonable to separately evaluate the association of gene polymorphisms with OSCC, oral adenocarcinoma and other cancer types.

To the best of our knowledge, this is the first meta-analysis to assess the association between the CYP1A1 MspI genetic variants and risks of OSCC. Although there are two previous meta-analyses (67,68) regarding the CYP1A1 MspI polymorphism and oral cancer, the results did not involve the single histopathological type and therefore cannot represent the association of CYP1A1 MspI with the risks of OSCC. Oral cancer is known to include different histological types, including squamous cell carcinoma and adenocarcinoma, which may yield to different susceptibilities of cancer. Therefore, the previous studies' results may regard all types of oral carcinoma for only one selection. To obtain a powerful conclusion regarding the risks of OSCC and CYP1A1 MspI polymorphism, a systematical meta-analysis was performed in the present study.

In the present meta-analysis, for the overall data the results of ORs and 95% CIs showed that the C allele of CYP1A1 MspI played a significant role in the carcinogenesis process resulting in OSCC, and as for the genotypes, CC and CT+CC were identified as risk factors for developing OSCC. All the results indicated that the CYP1A1 MspI polymorphism may increase the risks of OSCC. The heterogeneity among studies was observed in the dominant, recessive, additive and C versus T allele models, respectively. Following the subgroup analysis by ethnicity, the heterogeneity was not removed indicating that other factors, such as age, gender, country, source of controls, lifestyle, social status, smoking and alcohol habits, may also yield to heterogeneities.

In the subgroup analysis by ethnicity, a key association between the CYP1A1 MspI polymorphism and risks of OSCC in the Asian population was confirmed in all four models, but not in the mixed-race and Caucasian populations, suggesting that the CYP1A1 MspI gene variants may increase the OSCC susceptibility in the Asian population. The differences may be attributed to different ethnicities sharing different gene-gene and gene-environmental backgrounds. Nevertheless, the conclusion regarding the mixed-race and Caucasian populations is not of a sufficient power for the few studies and subjects.

Publication biases were evaluated by funnel plots and their symmetries, and were further assessed by Begg's test and Egger's linear regression tests, respectively. No clear biases were observed, indicating that the publication may yield to little effects on the results. The sensitivity analysis showed that the importance of the corresponding pooled ORs was not significantly changed, suggesting that the pooled ORs were stable.

However, several limitations should be addressed. First of all, the original studies included data regarding the Asian, Caucasian and mixed-race populations, and only one study regarding Caucasian and two mixed-race populations. Secondly, a subgroup analysis was performed by ethnicity, but the other factors, such as gender, age, source of control and country, were not performed due to data limitations. Thirdly, the Asian population included India, Japan and China, but other Asian countries were not included. Fourthly, heterogeneity existed, which may weaken the reliability of the conclusions. In view of these limitations, the results should be considered with caution.

Overall, despite several limitations the results of the present analysis showed a clear association between the CYP1A1 MspI polymorphism and OSCC risk, particularly among the Asian population. Future studies focusing on the CYP1A1 MspI polymorphism containing larger sample sizes and well-matched criteria are required to improve the credibility of the conclusions.

Acknowledgements

The present study was supported by Special Financial Grants from the China Postdoctoral Science Foundation (no. 2014T70836) and the National Natural Science Foundation of China (nos. 81371162, 8110762 and 30973336). The authors acknowledge Dr Wenjie Li (Department of Oral Health Sciences, School of Dentistry, University of Washington, Seattle, WA, USA) and Dr Xinchen Yang (Department of Oral Rehabilitation, Faculty of Dentistry, University of Hong Kong, Sai Ying Pun, Hong Kong, China) for assistance in collecting the relevant studies.

References

1 

Kademani D: Oral cancer. Mayo Clin Proc. 82:878–887. 2007. View Article : Google Scholar : PubMed/NCBI

2 

Petersen PE: Oral cancer prevention and control - the approach of the World Health Organization. Oral Oncol. 45:454–460. 2009. View Article : Google Scholar : PubMed/NCBI

3 

Barnes L, Eveson JW, Reichart P and Sidransky D: Tumours of the oral cavity and oropharynx. World Health Organization Classification of Tumours: Pathology and Genetics of Head and Neck Tumours. 9:(3rd). (Lyon, France). IARC Press. 166–210. 2005.

4 

Chen GS and Chen CH: A study on survival rates of oral squamous cell carcinoma. Kaohsiung J Med Sci. 12:317–325. 1996.(In Chinese). PubMed/NCBI

5 

Lim YC and Choi EC: Surgery alone for squamous cell carcinoma of the oral cavity: survival rates, recurrence patterns, and salvage treatment. Acta Otolaryngol. 128:1132–1137. 2008. View Article : Google Scholar : PubMed/NCBI

6 

Lo Muzio L, Campisi G, Farina A, et al: P-cadherin expression and survival rate in oral squamous cell carcinoma: an immunohistochemical study. BMC Cancer. 5:632005. View Article : Google Scholar : PubMed/NCBI

7 

Blot WJ, McLaughlin JK, Winn DM, et al: Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res. 48:3282–3287. 1988.PubMed/NCBI

8 

Ruiz Figuero E, Peláez Carretero MA, Lapiedra Cerero R, Gómez Esparza G and López Moreno LA: Effects of the consumption of alcohol in the oral cavity: relationship with oral cancer. Med Oral. 9:14–23. 2004.PubMed/NCBI

9 

Johnson N: Tobacco use and oral cancer: a global perspective. J Dent Educ. 65:328–339. 2001.PubMed/NCBI

10 

Zhang Y, Ni Y, Zhang H, Pan Y, Ma J and Wang L: Association between GSTM1 and GSTT1 allelic variants and head and neck squamous cell cancinoma. PLoS One. 7:e475792012. View Article : Google Scholar : PubMed/NCBI

11 

Wang Y, Yang H, Li L and Wang H: Glutathione S-transferase T1 gene deletion polymorphism and lung cancer risk in Chinese population: a meta-analysis. Cancer Epidemiol. 34:593–597. 2010. View Article : Google Scholar : PubMed/NCBI

12 

Pei YL, Zhang HL and Han HG: Polymorphism of 8q24 rsl3281615 and breast cancer risk: a meta-analysis. Tumor Biol. 34:421–428. 2013. View Article : Google Scholar

13 

Ji YN, Wang Q and Suo LJ: CYP1A1 Ile462Val polymorphism contributes to lung cancer susceptibility among lung squamous carcinoma and smokers: a meta-analysis. PloS One. 7:e433972012. View Article : Google Scholar : PubMed/NCBI

14 

Hashibe M, Brennan P, Strange RC, et al: Meta- and pooled analyses of GSTM1, GSTT1, GSTP1, and CYP1A1 genotypes and risk of head and neck cancer. Cancer Epidemiol Biomarkers Prev. 12:1509–1517. 2003.PubMed/NCBI

15 

Feng X, Zhou H-F, Zheng B-S, Shi J-J, Luo C and Qin J-J: Association of glutathione S-transferase P1 gene polymorphism with the histological types of lung cancer: a meta-analysis. Mol Biol Rep. 40:2439–2447. 2013. View Article : Google Scholar : PubMed/NCBI

16 

Tanimoto K, Hayashi S, Yoshiga K and Ichikawa T: Polymorphisms of the CYP1A1 and GSTM1 gene involved in oral squamous cell carcinoma in association with a cigarette dose. Oral Oncol. 35:191–196. 1999. View Article : Google Scholar : PubMed/NCBI

17 

Shukla D, Kale Dinesh A, Hallikerimath S, Vivekanandhan S and Venkatakanthaiah Y: Genetic polymorphism of drug metabolizing enzymes (GSTM1 and CYP1A1) as risk factors for oral premalignant lesions and oral cancer. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 156:253–259. 2012. View Article : Google Scholar : PubMed/NCBI

18 

Sato M, Sato T, Izumo T and Amagasa T: Genetic polymorphism of drug-metabolizing enzymes and susceptibility to oral cancer. Carcinogenesis. 20:1927–1931. 1999. View Article : Google Scholar : PubMed/NCBI

19 

Sam SS, Thomas V, Reddy KS, Surianarayanan G and Chandrasekaran A: CYP1A1 polymorphisms and the risk of upper aerodigestive tract cancers in an indian population. Head Neck. 30:1566–1574. 2008. View Article : Google Scholar : PubMed/NCBI

20 

Losi-Guembarovski R, Cólus IM, De Menezes RP, et al: Lack of association among polymorphic xenobiotic-metabolizing enzyme genotypes and the occurrence and progression of oral carcinoma in a brazilian population. Anticancer Res. 28:1023–1028. 2008.PubMed/NCBI

21 

Kao SY, Wu CH, Lin SC, et al: Genetic polymorphism of cytochrome P4501A1 and susceptibility to oral squamous cell carcinoma and oral precancer lesions associated with smoking/betel use. J Oral Pathol Med. 31:505–511. 2002. View Article : Google Scholar : PubMed/NCBI

22 

Gronau S, Koenig-Greger D, Jerg M and Riechelmann H: GSTM1 enzyme concentration and enzyme activity in correlation to the genotype of detoxification enzymes in squamous cell carcinoma of the oral cavity. Oral Dis. 9:62–67. 2003. View Article : Google Scholar : PubMed/NCBI

23 

Gattás GJ, de Carvalho MB, Siraque MS, et al: Genetic polymorphisms of CYP1A1, CYP2E1, GSTM1, and GSTT1 associated with head and neck cancer. Head Neck. 28:819–826. 2006. View Article : Google Scholar : PubMed/NCBI

24 

Cha IH, Park JY, Chung WY, Choi MA, Kim HJ and Park KK: Polymorphisms of CYP1A1 and GSTM1 genes and susceptibility to oral cancer. Yonsei Med J. 48:233–239. 2007. View Article : Google Scholar : PubMed/NCBI

25 

Anantharaman D, Chaubal PM, Kannan S, Bhisey RA and Mahimkar MB: Susceptibility to oral cancer by genetic polymorphisms at CYP1A1, GSTM1 and GSTT1 loci among indians: tobacco exposure as a risk modulator. Carcinogenesis. 28:1455–1462. 2007. View Article : Google Scholar : PubMed/NCBI

26 

Bartsch H, Nair U, Risch A, Rojas M, Wikman H and Alexandrov K: Genetic polymorphism of CYP genes, alone or in combination, as a risk modifier of tobacco-related cancers. Cancer Epidemiol Biomarkers Prev. 9:3–28. 2000.PubMed/NCBI

27 

Petersen DD, McKinney CE, Ikeya K, et al: Human CYP1A1 gene: cosegregation of the enzyme inducibility phenotype and an RFLP. Am J Hum Genet. 48:720–725. 1991.PubMed/NCBI

28 

Landi MT, Bertazzi PA, Shields PG, et al: Association between CYP1A1 genotype, mRNA expression and enzymatic activity in humans. Pharmacogenetics. 4:242–246. 1994. View Article : Google Scholar : PubMed/NCBI

29 

Zhou SF, Liu JP and Chowbay B: Polymorphism of human cytochrome P450 enzymes and its clinical impact. Drug Metab Rev. 41:89–295. 2009. View Article : Google Scholar : PubMed/NCBI

30 

Wells GA, Shea B, O'Connell D, Peterson J, Welch V, Losos M and Tugwell P: The Newcastle-Ottawa scale (NOS) for assessing the quality of nonrandomised studies in meta-analyses. simplehttp://www.ohri.ca/programs/clinical_epidemiology/oxford.aspAccessed. February 03–2016

31 

Stang A: Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol. 25:603–605. 2010. View Article : Google Scholar : PubMed/NCBI

32 

Cochran WG: The combination of estimates from different experiments. Biometrics. 10:101–129. 1954. View Article : Google Scholar

33 

Egger M, Smith Davey G, Schneider M and Minder C: Bias in meta-analysis detected by a simple, graphical test. BMJ. 315:629–634. 1997. View Article : Google Scholar : PubMed/NCBI

34 

Matthias C, Bockmühl U, Jahnke V, Harries LW, Wolf CR, et al: The glutathione S-transferase GSTP1 polymorphism: effects on susceptibility to oral/pharyngeal and laryngeal carcinomas. Pharmacogenetics. 8:1–6. 1998. View Article : Google Scholar : PubMed/NCBI

35 

Khlifi R, Messaoud O, Rebai A and Hamza-Chaffai A: Polymorphisms in the human cytochrome P450 and arylamine N-Acetyltransferase: susceptibility to head and neck cancers. Biomed Res Int. 2013:5827682013. View Article : Google Scholar : PubMed/NCBI

36 

Liu L, Wu G, Xue F, et al: Functional CYP1A1 genetic variants, alone and in combination with smoking, contribute to development of head and neck cancers. Eur J Cancer. 49:2143–2151. 2013. View Article : Google Scholar : PubMed/NCBI

37 

Ruwali M and Parmar D: Association of functionally important polymorphisms in cytochrome P450s with squamous cell carcinoma of head and neck. Indian J Exp Biol. 48:651–665. 2010.PubMed/NCBI

38 

Amtha R, Ching CS, Zain R, et al: GSTM1, GSTT1 and CYP1A1 polymorphisms and risk of oral cancer: a case-control study in Jakarta, Indonesia. Asian Pac J Cancer Prev. 10:21–26. 2009.PubMed/NCBI

39 

Buch SC, Nazar-Stewart V, Weissfeld JL and Romkes M: Case-control study of oral and oropharyngeal cancer in whites and genetic variation in eight metabolic enzymes. Head Neck. 30:1139–1147. 2008. View Article : Google Scholar : PubMed/NCBI

40 

Katoh T: Application of molecular biology to occupational health field - the frequency of gene polymorphism of cytochrome P450 1A1 and glutathione S-transferase M1 in patients with lung, oral and urothelial cancer. J UOEH. 17:271–278. 1995.(In Japanese). PubMed/NCBI

41 

Katoh T, Kaneko S, Kohshi K, et al: Genetic polymorphisms of tobacco- and alcohol-related metabolizing enzymes and oral cavity cancer. Int J Cancer. 83:606–609. 1999. View Article : Google Scholar : PubMed/NCBI

42 

Marques CF, Koifman S, Koifman RJ, Boffetta P, Brennan P and Hatagima A: Influence of cyp1a1, CYP2E1, GSTM3 and NAT2 genetic polymorphisms in oral cancer susceptibility: results from a case-control study in Rio de Janeiro. Oral Oncol. 42:632–637. 2006. View Article : Google Scholar : PubMed/NCBI

43 

Sugimura T, Kumimoto H, Tohnai I, et al: Gene-environment interaction involved in oral carcinogenesis: molecular epidemiological study for metabolic and DNA repair gene polymorphisms. J Oral Pathol Med. 35:11–18. 2006. View Article : Google Scholar : PubMed/NCBI

44 

Shukla D, Kale AD, Hallikerimath S, Yerramalla V, Subbiah V and Mishra S: Association between GSTM1 and CYP1A1 polymorphisms and survival in oral cancer patients. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 157:304–310. 2013.PubMed/NCBI

45 

Anantharaman D, Samant TA, Sen S and Mahimkar MB: Polymorphisms in tobacco metabolism and DNA repair genes modulate oral precancer and cancer risk. Oral Oncol. 47:866–872. 2011. View Article : Google Scholar : PubMed/NCBI

46 

Boccia S, Cadoni G, Sayed-Tabatabaei FA, et al: CYP1A1, CYP2E1, GSTM1, GSTT1, EPHX1 exons 3 and 4, and NAT2 polymorphisms, smoking, consumption of alcohol and fruit and vegetables and risk of head and neck cancer. J Cancer Res Clin Oncol. 134:93–100. 2008. View Article : Google Scholar : PubMed/NCBI

47 

Canova C, Richiardi L, Merletti F, et al: Alcohol, tobacco and genetic susceptibility in relation to cancers of the upper aerodigestive tract in northern Italy. Tumori. 96:1–10. 2010.PubMed/NCBI

48 

Cury NM, Russo A, Galbiatti ALS, et al: Polymorphisms of the CYP1A1 and CYP2E1 genes in head and neck squamous cell carcinoma risk. Mol Biol Rep. 39:1055–1063. 2012. View Article : Google Scholar : PubMed/NCBI

49 

Ko Y, Abel J, Harth V, et al: Association of CYP1B1 codon 432 mutant allele in head and neck squamous cell cancer is reflected by somatic mutations of p53 in tumor tissue. Cancer Res. 61:4398–4404. 2001.PubMed/NCBI

50 

Olivieri EH, da Silva SD, Mendonca FF, et al: CYP1A2*1C, CYP2E1*5B, and GSTM1 polymorphisms are predictors of risk and poor outcome in head and neck squamous cell carcinoma patients. Oral Oncol. 45:e73–e79. 2009. View Article : Google Scholar : PubMed/NCBI

51 

Ramadas K, Ramachandran S, Muwonge R and Pillai MR: Tumor progression in the oral cavity: The significance of genetic polymorphisms in CYP1A1, GST M1 and XRCC1 in a south Indian population. Oral Oncol Supplement. (Suppl 3): 69. 2009. View Article : Google Scholar

52 

Sabitha K, Reddy MV and Jamil K: Smoking related risk involved in individuals carrying genetic variants of CYP1A1 gene in head and neck cancer. Cancer Epidemiol. 34:587–592. 2010. View Article : Google Scholar : PubMed/NCBI

53 

Sam SS, Thomas V, Reddy KS, Surianarayanan G and Chandrasekaran A: Gene-gene interactions of drug metabolizing enzymes and transporter protein in the risk of upper aerodigestive tract cancers among indians. Cancer Epidemiol. 34:626–633. 2010. View Article : Google Scholar : PubMed/NCBI

54 

Sam SS, Thomas V, Reddy KS, Surianarayanan G and Chandrasekaran A: Gene-environment interactions associated with CYP1A1 Mspi and GST polymorphisms and the risk of upper aerodigestive tract cancers in an indian population. J Cancer Res Clin Oncol. 136:945–951. 2010. View Article : Google Scholar : PubMed/NCBI

55 

Sharma R, Ahuja M, Panda NK and Khullar M: Combined effect of smoking and polymorphisms in tobacco carcinogen-metabolizing enzymes CYP1A1 and GSTM1 on the head and neck cancer risk in North Indians. DNA Cell Biol. 29:441–448. 2010. View Article : Google Scholar : PubMed/NCBI

56 

Sharma R, Ahuja M, Panda NK and Khullar M: Interactions among genetic variants in tobacco metabolizing genes and smoking are associated with head and neck cancer susceptibility in North Indians. DNA Cell Biol. 30:611–616. 2011. View Article : Google Scholar : PubMed/NCBI

57 

Sharma R, Panda NK and Khullar M: Hypermethylation of carcinogen metabolism genes, CYP1A1, CYP2A13 and GSTM1 genes in head and neck cancer. Oral Dis. 16:668–673. 2010. View Article : Google Scholar : PubMed/NCBI

58 

Singh AP, Shah PP, Ruwali M, Mathur N, Pant MC and Parmar D: Polymorphism in cytochrome P4501A1 is significantly associated with head and neck cancer risk. Cancer Invest. 27:869–876. 2009. View Article : Google Scholar : PubMed/NCBI

59 

Yadav SS, Ruwali M, Pant MC, Shukla P, Singh RL and Parmar D: Interaction of drug metabolizing cytochrome P450 2D6 poor metabolizers with cytochrome P450 2C9 and 2C19 genotypes modify the susceptibility to head and neck cancer and treatment response. Mutat Res. 684:49–55. 2010. View Article : Google Scholar : PubMed/NCBI

60 

Chatterjee S, Dhar S, Sengupta B, et al: Polymorphisms of CYP1A1, GSTM1 and GSTT1 loci as the genetic predispositions of oral cancers and other oral pathologies: tobacco and alcohol as risk modifiers. Indian J Clin Biochem. 25:260–272. 2010. View Article : Google Scholar : PubMed/NCBI

61 

Cordero K, Espinoza I, Caceres D, et al: Oral cancer susceptibility associated with the CYP1A1 and GSTM1 genotypes in Chilean individuals. Oncol Lett. 1:549–553. 2010.PubMed/NCBI

62 

Guo L, Zhang C, Shi S and Guo X: Correlation between smoking and the polymorphisms of cytochrome P450 1A1-Msp I and glutathione s-transferase T1 genes and oral cancer. Hua Xi Kou Qiang Yi Xue Za Zhi. 30:187–191. 2012.(In Chinese). PubMed/NCBI

63 

Masood N, Kayani MA, Malik FA, Mahjabeen I, Baig RM and Faryal R: Genetic variations in carcinogen metabolizing genes associated with oral cancer in pakistani population. Asian Pac J Cancer Prev. 12:491–495. 2011.PubMed/NCBI

64 

Matthias C, Bockmühl U, Jahnke V, et al: Polymorphism in cytochrome P450 CYP2D6, CYP1A1, CYP2E1 and glutathione S-transferase, GSTM1, GSTM3, GSTT1 and susceptibility to tobacco-related cancers: studies in upper aerodigestive tract cancers. Pharmacogenetics. 8:91–100. 1998. View Article : Google Scholar : PubMed/NCBI

65 

Chatterjee S, Chakrabarti S, Sengupta B, et al: Prevalence of CYP1A1 and GST polymorphisms in the population of northeastern India and susceptibility of oral cancer. Oncol Res. 17:397–403. 2009. View Article : Google Scholar : PubMed/NCBI

66 

Zhan P, Wang Q, Qian Q, Wei S-Z and Yu L-K: CYP1A1 MspI and exon7 gene polymorphisms and lung cancer risk: an updated meta-analysis and review. J Exp Clin Cancer Res. 30:992011. View Article : Google Scholar : PubMed/NCBI

67 

Zhuo W, Wang Y, Zhuo X, et al: CYP1A1 and GSTM1 polymorphisms and oral cancer risk: association studies via evidence-based meta-analyses. Cancer Invest. 27:86–95. 2009. View Article : Google Scholar : PubMed/NCBI

68 

Zhuo X, Zhao H, Chang A, et al: Quantitative assessment of CYP1A1*2A variations with oral carcinoma susceptibility: evidence from 1,438 cases and 2,086 controls. Cancer Invest. 30:552–559. 2012. View Article : Google Scholar : PubMed/NCBI

Related Articles

Journal Cover

April 2016
Volume 4 Issue 4

Print ISSN: 2049-9450
Online ISSN:2049-9469

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
APA
Xie, S., Luo, C., Shan, X., Zhao, S., He, J., & Cai, Z. (2016). CYP1A1 MspI polymorphism and the risk of oral squamous cell carcinoma: Evidence from a meta‑analysis. Molecular and Clinical Oncology, 4, 660-666. https://doi.org/10.3892/mco.2016.768
MLA
Xie, S., Luo, C., Shan, X., Zhao, S., He, J., Cai, Z."CYP1A1 MspI polymorphism and the risk of oral squamous cell carcinoma: Evidence from a meta‑analysis". Molecular and Clinical Oncology 4.4 (2016): 660-666.
Chicago
Xie, S., Luo, C., Shan, X., Zhao, S., He, J., Cai, Z."CYP1A1 MspI polymorphism and the risk of oral squamous cell carcinoma: Evidence from a meta‑analysis". Molecular and Clinical Oncology 4, no. 4 (2016): 660-666. https://doi.org/10.3892/mco.2016.768