Journal Logo

Research Article: Systematic Review and Meta-Analysis

Association of CYP1A1 and GSTM1 Polymorphisms With Oral Cancer Susceptibility

A Meta-Analysis

Liu, Haitao MM; Jia, Jinlin MM; Mao, Xuemei MM; Lin, Zhiyong MM

Section Editor(s): Li., Jianfeng

Author Information
doi: 10.1097/MD.0000000000000895
  • Open



Oral cancer is one of the most common cancers in the world,1 the incidence of which has increased obviously in the last few years among different populations.2,3 It is generally considered that genetic polymorphisms and environmental factors including cigarette smoking, alcohol consumption, and betel quid chewing are of particular importance in the etiology of oral cancer.4,5

Genetic polymorphisms is prevalent and play a viral role in human diseases. Recently, the relationship of genetic polymorphisms and the risk of cancers have been researched widely. Among the genes, cytochrome P450 1A1 (also known as CYP1A1) gene, located on chromosome 15, encodes aryl hydrocarbon hydrolase, which involves in metabolism of polycyclic aromatic hydrocarbons (PAHs).6 For CYP1A1, rs4646903 polymorphism, a T to C transition in the 3′ noncoding region (a thymine/cytosine point mutation), has been confirmed to be related with the high risk of lung and head and neck cancers.7,8 In addition, CYP1A1 rs1048943 polymorphism, an amino acid substitution from isoleucine to valine at codon 462, shows the effects of enhancing catalytic activity and increasing the risk for lung cancer.9,10 For glutathione-S-transferase M1 (GSTM1), the polymorphism includes present genotype and null genotype, which are associated with abnormal function of GSTμ enzyme that is an important member in the detoxification of carcinogens in tobacco smoking.11,12 Moreover, the null genotype was reported to associate with increased risk of gastric, bladder, colon, and lung cancers.13–16 It is worth mentioning that CYP1A1, phase I enzyme, and GSTM1, phase II enzyme, could affect individual variability in the metabolism of chemical substances and finally affect the susceptibility to cancers through increasing the activity of xenobiotic metabolizing enzymes.17–20

Up to now, several epidemiological studies have focused on the association of CYP1A1 and GSTM1 polymorphisms with oral cancer susceptibility.2,21–69 However, the results remained conflicting. Therefore, the meta-analysis was carried out to gain more comprehensive evidences for the association.


Search Strategy

The relevant articles were searched in PubMed, Embase, and CNKI databases using the keywords “CYP1A1” or “cytochrome P450 1A1,” “GSTM1” or “glutathione-S-transferase M1,” “polymorphism,” and “oral cancer.” The reference lists in retrieved papers were also screened manually for potential articles. All the selected studies should comply with the following inclusion criteria: case–control studies, studies about the association of CYP1A1 and GSTM1 polymorphisms with oral cancer susceptibility, and adequate data for estimating an odds ratio (OR) with 95% confidence interval (CI). When the same data existed in >1 publication, the largest or most recent publication was included. This study is a meta-analysis and does not involve populations; ethical approval was not required.

Data Extraction

The following data were extracted from each study by 2 independent investigators: name of first author, publication date, country of origin, ethnicity, source of controls, genotyping methods, total number of cases and controls, genotype frequencies in case and control groups and Hardy–Weinberg equilibrium (HWE). Disagreements were solved by a discussion between the 2 investigators. The characteristics of the included articles were shown in Tables 1 and 2.

Characteristics of Studies on CYP1A1 Polymorphisms
Principle Characteristics of Studies on GSTM1 Null/Present

Statistical Analysis

We applied crude ORs with corresponding 95% CIs to evaluate the association of CYP1A1 and GSTM1 polymorphisms with oral cancer susceptibility. Heterogeneity assumption was estimated by the χ2-based Q test. When P < 0.05, which indicated significant heterogeneity among studies, the pooled OR was calculated using the random-effects model; otherwise, the fixed-effects model was used. The pooled results of CYP1A1 were analyzed under the following genetic models: 22 versus 11, 22 + 12 versus 11, 22 versus 11 + 12, 2 versus 1, and 12 versus 11. For GSTM1, null versus present and present versus null models were used. Sensitivity analysis was conducted to measure the stability of pooled results. Publication bias was assessed by Begg funnel plot and Egger test. HWE was checked by χ2 test. Statistical data were performed using the STATA software (version 12.0; Stata Corporation, Texas, Tex, USA).


Study Characteristics

As displayed in Figure 1, a total of 243 articles were searched through databases in which 132 articles were excluded for obvious irrelevance, 34 articles were excluded for unrelated single nucleotide polymorphisms (SNPs), and 27 articles were eliminated for not having controls and original genotype data. Finally, 50 articles were included in our meta-analysis.2,21–69

Flow diagram of included studies for the meta-analysis. CNKI = China National Knowledge Infrastructure, SNP = single nucleotide polymorphism.


The results were shown in Tables 3 and 4. Overall, CYP1A1 rs4646903 polymorphism was closely associated with the increased risk of oral cancer according to the pooled ORs (CC vs TT: OR 1.65, 95% CI 1.33–2.05; CC vs TC+TT: OR 1.77, 95% CI 1.48–2.11; C vs T: OR 1.17, 95% CI 1.07–1.28). Using the CC+TC versus TT model and the TC versus TT model, we did not find any significant association (Table 3). Subgroup analysis by ethnicity showed similar association of rs4646903 with oral cancer in Asians in the same genetic models tested (CC vs TT: OR 1.70, 95% CI 1.35–2.13; CC vs TC+TT: OR 1.83, 95% CI 1.52–2.20; C vs T: OR 1.17, 95% CI 1.06–1.29) but not in whites. Further subgroup analysis by source of control revealed that rs4646903 was significantly related with oral cancer susceptibility in hospital-based population (CC vs TT: OR 1.53, 95% CI 1.15–2.05; CC vs TC+TT: OR 1.67, 95% CI 1.26–2.20) and population-based population (CC vs TT: OR 1.81, 95% CI 1.31–2.51; CC+TC vs TT: OR 1.23, 95% CI 1.04–1.46; CC vs TC+TT: OR 1.84, 95% CI 1.46–2.32; C vs T: OR 1.26, 95% CI 1.09–1.46), as shown in Figure 2. For CYP1A1 rs1048943, subgroup analysis by ethnicity indicated that it was related with increased risk of oral cancer in Asians (GG vs AA: OR 1.91, 95% CI 1.20–3.04; GG vs GA+AA: OR 1.76, 95% CI 1.10–2.80; G vs A: OR 1.27, 95% CI 1.07–1.50) but not in whites and other ethnic groups (Figure 3). However, no significant relationship was found between the CYP1A1 rs1048943 polymorphism and oral cancer risk in overall analysis and subgroup analysis by source of control.

CYP1A1 Polymorphisms and Oral Cancer Risk
GSTM1 Null/Present and Oral Cancer Risk
Forest plot of oral cancer susceptibility associated with CYP1A1 rs4646903 polymorphism under CC versus TT genetic model. CI = confidence interval, OR = odds ratio.
Forest plot of oral cancer risk related to CYP1A1 rs1048943 polymorphism in Asians under GG versus AA genetic model. CI = confidence interval, OR = odds ratio.

With respect to GSTM1 polymorphisms, null genotype showed obvious relevance to oral cancer susceptibility (OR 1.23, 95% CI 1.12–1.34), especially in Asians (OR 1.27, 95% CI 1.15–1.41), compared with present genotype. Moreover, it was demonstrated that null genotype could affect individual susceptibility to oral cancer in both hospital- and population-based populations (OR 1.11, 95% CI 1.01–1.21; OR 1.38, 95% CI 1.18–1.61), as displayed in Figure 4.

Forest plot of oral cancer risk associated with GSTM1 null/present. For each study, the estimates of OR and its 95% CI are plotted with square and a horizontal line. The area of the squares reflects the weight (inverse of the variance). The diamond represents the summary OR and 95% CI. GSTM1 = glutathione-S-transferase M1, CI = confidence interval, OR = odds ratio.

Sensitivity Analysis

Sensitivity analysis was performed to evaluate the influence of each individual study on the pooled ORs. The recalculated ORs were not substantially influenced, which suggested our results were stable.

Publication Bias

Egger test and Begg funnel plot were conducted to estimate publication bias. The shape of the funnel plot was relatively symmetrical (Figure 5). Additionally, the result of Egger test did not show statistical evidence for bias (P = 0.656). Thus, there was no obvious publication bias in our meta-analysis, and the results were credible.

Begg funnel plot of publication bias. Each point represents a separate study for the indicated association. Log (OR), natural logarithm of OR; horizontal line, mean effect size. CI = confidence interval, OR = odds ratio.


Oral cancer has become a major health problem characterized by high incidence, poor survival rate, and severe functional and cosmetic defects accompanying the treatment.70 Moreover, it has been demonstrated that genetic and environmental factors could affect individual susceptibility to oral cancer. Therefore, it is significant to investigate the association of CYP1A1 and GSTM1 polymorphisms with oral cancer risk.

CYP1A1 rs4646903 and rs1048943 polymorphisms contribute to increased enzyme activity of CYP1A1 and are crucial to the activation of PAHs.6,39 The null genotype of GSTM1 polymorphism could result in the inactivation of GSTM1 enzyme and thus decrease the capacity of detoxifying carcinogens.71 So far, several epidemiological studies have evaluated the association of CYP1A1 and GSTM1 polymorphisms with oral cancer susceptibility. In our study, CYP1A1 rs4646903 was verified to increase the risk of oral cancer, particularly in Asians, whereas CYP1A1 rs1048943 polymorphism did not show significant relationship with oral cancer susceptibility, when we pooled all data together, but demonstrated a statistically significant association when data were limited to Asians, which was consistent with the results of most previous studies.2,24,37,40,45,47,53,56,58,71,72 However, there were some studies with opposite results to ours. Among them, Losi-Guembarovski et al51 and Amtha et al58 found that there was no significant association between CYP1A1 rs4646903 polymorphism and oral cancer risk. In the studies of Katoh et al38 and Sreelekha et al,39CYP1A1 rs1048943 showed no association with the susceptibility of oral cancer. Compared with the above studies, our study showed advantages in population composed of Asians, whites, and other ethnic groups and relatively lager sample size, which make our result much more credible.

For the association between null genotype of GSTM1 polymorphisms and oral cancer risk, the results were also not conclusive.25–31,33,34,41,44,63,65,66,68,73,74 Our meta-analysis demonstrated that null genotype of GSTM1 polymorphisms was significantly associated with overall risk of oral cancer. However, the significance was lost in further analysis among whites.

The 3 polymorphisms analyzed in the present work have 1 thing in common. None of them demonstrated a significant association with genetic risk of oral cancer in whites. The null results may be biased because the current sample is insufficient to determine whether there is an association in this population. Another possibility is that both CYP1A1 and GSTM1 polymorphisms modify oral cancer risk in an ethnic-specific fashion due to different genetic backgrounds. These possibilities clearly require to be investigated in future research.

Certain limitations in our study should be noted. First, our study was not stratified by smoking status, which was identified as a key factor in oral cancer risk.54 Second, subgroup analysis of CYP1A1 polymorphisms involved relatively fewer data in whites and other ethnic groups, which may produce some bias in the results. Finally, lack of original data about present genotype of GSTM1 polymorphisms might influence the combined results.

In conclusion, our meta-analysis indicates that CYP1A1 rs4646903, rs1048943, and null genotype of GSTM1 polymorphisms are possible risk factors for oral cancer, especially in Asians. In the future, in-depth studies are required to further explore the association.


1. Petersen PE. Oral cancer prevention and control—the approach of the World Health Organization. Oral Oncol 2009; 45:454–460.
2. Sato M, Sato T, Izumo T, et al. Genetic polymorphism of drug-metabolizing enzymes and susceptibility to oral cancer. Carcinogenesis 1999; 20:1927–1931.
3. Masood N, Yasmin A, Kayani MA. Genetic deletions of GSTM1 and GSTT1 in head and neck cancer: review of the literature from 2000 to 2012. Asian Pac J Cancer Prev 2013; 14:3535–3539.
4. Zygogianni AG, Kyrgias G, Karakitsos P, et al. Oral squamous cell cancer: early detection and the role of alcohol and smoking. Head Neck Oncol 2011; 3:2.
5. Reichart PA, Nguyen XH. Betel quid chewing, oral cancer and other oral mucosal diseases in Vietnam: a review. J Oral Pathol Med 2008; 37:511–514.
6. Nebert DW, Nelson DR, Coon MJ, et al. The P450 superfamily: update on new sequences, gene mapping, and recommended nomenclature. DNA Cell Biol 1991; 10:1–14.
7. Kawajiri K, Nakachi K, Imai K, et al. Identification of genetically high risk individuals to lung cancer by DNA polymorphisms of the cytochrome P450IA1 gene. FEBS Lett 1990; 263:131–133.
8. 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 2003; 12:1509–1517.
9. Hayashi SI, Watanabe J, Nakachi K, et al. PCR detection of an A/G polymorphism within exon 7 of the CYP1A1 gene. Nucleic Acids Res 1991; 19:4797.
10. Kawajiri K, Eguchi H, Nakachi K, et al. Association of CYP1A1 germ line polymorphisms with mutations of the p53 gene in lung cancer. Cancer Res 1996; 56:72–76.
11. Wolf CR. Metabolic factors in cancer susceptibility. Cancer Surv 1990; 9:437–474.
12. Harada S, Abei M, Tanaka N, et al. Liver glutathione S-transferase polymorphism in Japanese and its pharmacogenetic importance. Hum Genet 1987; 75:322–325.
13. Lafuente A, Pujol F, Carretero P, et al. Human glutathione S-transferase mu (GST mu) deficiency as a marker for the susceptibility to bladder and larynx cancer among smokers. Cancer Lett 1993; 68:49–54.
14. Katoh T, Nagata N, Kuroda Y, et al. Glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) genetic polymorphism and susceptibility to gastric and colorectal adenocarcinoma. Carcinogenesis 1996; 17:1855–1859.
15. Zhong S, Wyllie AH, Barnes D, et al. Relationship between the GSTM1 genetic polymorphism and susceptibility to bladder, breast and colon cancer. Carcinogenesis 1993; 14:1821–1824.
16. Seidegard J, Pero RW, Miller DG, et al. A glutathione transferase in human leukocytes as a marker for the susceptibility to lung cancer. Carcinogenesis 1986; 7:751–753.
17. Hatagima A. Genetic polymorphisms and metabolism of endocrine disruptors in cancer susceptibility. Cad Saude Publica 2002; 18:357–377.
18. Nebert DW, McKinnon RA, Puga A. Human drug-metabolizing enzyme polymorphisms: effects on risk of toxicity and cancer. DNA Cell Biol 1996; 15:273–280.
19. Gonzalez FJ. The role of carcinogen-metabolizing enzyme polymorphisms in cancer susceptibility. Reprod Toxicol 1997; 11:397–412.
20. Moon KS, Lee HJ, Hong SH, et al. CYP1A1 and GSTM1/T1 genetic variation in predicting risk for cerebral infarction. J Mol Neurosci 2007; 32:155–159.
21. Sato M, Sato T, Izumo T, et al. Genetically high susceptibility to oral squamous cell carcinoma in terms of combined genotyping of CYP1A1 and GSTM1 genes. Oral Oncol 2000; 36:267–271.
22. Haile MJ, Wiggers JH, D Spigelman A, et al. Novel strategy to stop cigarette smoking by surgical patients: pilot study in a preadmission clinic. ANZ J Surg 2002; 72:618–622.
23. Al-Qudah HS, Santucci RA. Complications of renal trauma. Urol Clin North Am 2006; 33:41–53.
24. Leichsenring A, Losi-Guembarovski R, Maciel ME, et al. CYP1A1 and GSTP1 polymorphisms in an oral cancer case–control study. Braz J Med Biol Res 2006; 39:1569–1574.
25. Deakin M, Elder J, Hendrickse C, et al. Glutathione S-transferase GSTT1 genotypes and susceptibility to cancer: studies of interactions with GSTM1 in lung, oral, gastric, and colorectal cancers. Carcinogenesis 1996; 17:881–884.
26. Jourenkova-Mironova N, Voho A, Bouchardy C, et al. Glutathione S-transferase GSTM1, GSTM3, GSTP1 and GSTT1 genotypes and the risk of smoking-related oral and pharyngeal cancers. Int J Cancer 1999; 81:44–48.
27. Park LY, Muscat JE, Kaur T, et al. Comparison of GSTM polymorphisms and risk for oral cancer between African-Americans and Caucasians. Pharmacogenetics 2000; 10:123–131.
28. Kietthubthew S, Sriplung H, Au WW. Genetic and environmental interactions on oral cancer in Southern Thailand. Environ Mol Mutagen 2001; 37:111–116.
29. Buch SC, Notani PN, Bhisey RA. Polymorphism at GSTM1, GSTM3 and GSTT1 gene loci and susceptibility to oral cancer in an Indian population. Carcinogenesis 2002; 23:803–807.
30. Drummond SN, De Marco L, Noronha JC, et al. GSTM1 polymorphism and oral squamous cell carcinoma. Oral Oncol 2004; 40:52–55.
31. Sikdar N, Paul RR, Roy B. Glutathione S-transferase M3 (A/A) genotype as a risk factor for oral cancer and leukoplakia among Indian tobacco smokers. Int J Cancer 2004; 109:95–101.
32. Liu CJ, Chang CS, Lui MT, et al. Association of GST genotypes with age of onset and lymph node metastasis in oral squamous cell carcinoma. J Oral Pathol Med 2005; 34:473–477.
33. Sharma A, Mishra A, Das BC, et al. Genetic polymorphism at GSTM1 and GSTT1 gene loci and susceptibility to oral cancer. Neoplasma 2006; 53:309–315.
34. Hatagima A, Costa EC, Marques CF, et al. Glutathione S-transferase polymorphisms and oral cancer: a case–control study in Rio de Janeiro, Brazil. Oral Oncol 2008; 44:200–207.
35. Huang P, An YD, Wu C, et al. The preliminary study of GSTT1 and GSTM1 polymorphisms in oral and maxillofacial malignancy. J Pract Oncol 2006; 21:39–42.
36. Park JY, Muscat JE, Ren Q, et al. CYP1A1 and GSTM1 polymorphisms and oral cancer risk. Cancer Epidemiol Biomarkers Prev 1997; 6:791–797.
37. Tanimoto K, Hayashi S, Yoshiga K, et al. Polymorphisms of the CYP1A1 and GSTM1 gene involved in oral squamous cell carcinoma in association with a cigarette dose. Oral Oncol 1999; 35:191–196.
38. Katoh T, Kaneko S, Kohshi K, et al. Genetic polymorphisms of tobacco- and alcohol-related metabolizing enzymes and oral cavity cancer. Int J Cancer 1999; 83:606–609.
39. Sreelekha TT, Ramadas K, Pandey M, et al. Genetic polymorphism of CYP1A1, GSTM1 and GSTT1 genes in Indian oral cancer. Oral Oncol 2001; 37:593–598.
40. Hahn M, Hagedorn G, Kuhlisch E, et al. Genetic polymorphisms of drug-metabolizing enzymes and susceptibility to oral cavity cancer. Oral Oncol 2002; 38:486–490.
41. Gronau S, Koenig-Greger D, Jerg M, et al. GSTM1 enzyme concentration and enzyme activity in correlation to the genotype of detoxification enzymes in squamous cell carcinoma of the oral cavity. Oral Dis 2003; 9:62–67.
42. Xie H, Hou L, Shields PG, et al. Metabolic polymorphisms, smoking, and oral cancer in Puerto Rico. Oncol Res 2004; 14:315–320.
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 2006; 35:11–18.
44. Gattas GJ, de Carvalho MB, Siraque MS, et al. Genetic polymorphisms of CYP1A1, CYP2E1, GSTM1, and GSTT1 associated with head and neck cancer. Head Neck 2006; 28:819–826.
45. Cha IH, Park JY, Chung WY, et al. Polymorphisms of CYP1A1 and GSTM1 genes and susceptibility to oral cancer. Yonsei Med J 2007; 48:233–239.
46. Matthias C, Bockmuhl 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 1998; 8:91–100.
47. Varela-Lema L, Taioli E, Ruano-Ravina A, et al. Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review. Genet Med 2008; 10:369–384.
48. Coutelle C, Ward PJ, Fleury B, et al. Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms. Hum Genet 1997; 99:319–325.
49. Nomura T, Noma H, Shibahara T, et al. Aldehyde dehydrogenase 2 and glutathione S-transferase M 1 polymorphisms in relation to the risk for oral cancer in Japanese drinkers. Oral Oncol 2000; 36:42–46.
50. Hung HC, Chuang J, Chien YC, et al. Genetic polymorphisms of CYP2E1, GSTM1, and GSTT1; environmental factors and risk of oral cancer. Cancer Epidemiol Biomarkers Prev 1997; 6:901–905.
51. Losi-Guembarovski R, Colus 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 2008; 28:1023–1028.
52. 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 2010; 25:260–272.
53. Guo L, Zhang C, Shi S, et al. 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 2012; 30:187–191.
54. Majumder M, Sikdar N, Paul RR, et al. Increased risk of oral leukoplakia and cancer among mixed tobacco users carrying XRCC1 variant haplotypes and cancer among smokers carrying two risk genotypes: one on each of two loci, GSTM3 and XRCC1 (Codon 280). Cancer Epidemiol Biomarkers Prev 2005; 14:2106–2112.
55. Anantharaman D, Chaubal PM, Kannan S, et al. Susceptibility to oral cancer by genetic polymorphisms at CYP1A1, GSTM1 and GSTT1 loci among Indians: tobacco exposure as a risk modulator. Carcinogenesis 2007; 28:1455–1462.
56. Varela-Lema L, Ruano-Ravina A, Juiz Crespo MA, et al. CYP1A1, mEH, and GSTM1 polymorphisms and risk of oral and pharyngeal cancer: a Spanish case–control study. J Oncol 2008; 2008:741310.
57. Bathi RJ, Rao R, Mutalik S. GST null genotype and antioxidants: risk indicators for oral pre-cancer and cancer. Indian J Dent Res 2009; 20:298–303.
58. 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 2009; 10:21–26.
59. Cordero K, Espinoza I, Caceres D, et al. Oral cancer susceptibility associated with the CYP1A1 and GSTM1 genotypes in Chilean individuals. Oncol Lett 2010; 1:549–553.
60. Lourenco GJ, Silva EF, Rinck-Junior JA, et al. CYP1A1, GSTM1 and GSTT1 polymorphisms, tobacco and alcohol status and risk of head and neck squamous cell carcinoma. Tumour Biol 2011; 32:1209–1215.
61. Sharma R, Ahuja M, Panda NK, et al. 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 2010; 29:441–448.
62. Chen MK, Tsai HT, Chung TT, et al. Glutathione S-transferase P1 and alpha gene variants; role in susceptibility and tumor size development of oral cancer. Head Neck 2010; 32:1079–1087.
63. Shukla D, Dinesh Kale A, Hallikerimath S, et al. 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 2012; 156:253–259.
64. Masood N, Kayani MA, Malik FA, et al. Genetic variation in carcinogen metabolizing genes associated with oral cancer in Pakistani population. Asian Pac J Cancer Prev 2011; 12:491–495.
65. Yadav DS, Devi TR, Ihsan R, et al. Polymorphisms of glutathione-S-transferase genes and the risk of aerodigestive tract cancers in the Northeast Indian population. Genet Test Mol Biomarkers 2010; 14:715–723.
66. Delfino AE, Chandratilake M, Altermatt FR, et al. Validation and piloting of direct observation of practical skills tool to assess intubation in the Chilean context. Med Teach 2013; 35:231–236.
67. Mondal R, Ghosh SK, Choudhury JH, et al. Mitochondrial DNA copy number and risk of oral cancer: a report from Northeast India. PLoS One 2013; 8:e57771.
68. Shukla D, Dinesh Kale A, Hallikerimath S, et al. Association between GSTM1 and CYP1A1 polymorphisms and survival in oral cancer patients. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2013; 157:304–310.
69. Zhang C, Guo L, Guo X. Correlation of the polymorphism of EC-SOD and GSTM1 and smoking with oral cancer risk. Wei Sheng Yan Jiu 2012; 41:555–561.
70. Parkin DM, Bray F, Ferlay J, et al. Global cancer statistics, 2002. CA Cancer J Clin 2005; 55:74–108.
71. Yu KT, Ge C, Xu XF, et al. CYP1A1 polymorphism interactions with smoking status in oral cancer risk: evidence from epidemiological studies. Tumour Biol 2014; 35:11183–11191.
72. 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 2009; 27:86–95.
73. Zhao SF, Yang XD, Lu MX, et al. GSTM1 null polymorphisms and oral cancer risk: a meta-analysis. Tumour Biol 2014; 35:287–293.
74. Peng J, Liu HZ, Zhu YJ. Null glutathione S-transferase T1 and M1 genotypes and oral cancer susceptibility in China and India—a meta-analysis. Asian Pac J Cancer Prev 2014; 15:287–290.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.