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 ORIGINAL ARTICLE
Year : 2014  |  Volume : 51  |  Issue : 2  |  Page : 154-158

Role of CYP2E1genetic polymorphism in the development of oral leukoplakia among tobacco users in North Indian population


1 Department of Oral Pathology, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of General Surgery, Carrier Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Correspondence Address:
S Gupta
Department of Oral Pathology, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.138266

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Aim: The aim of the study to find out role of CYP2E1 genetic polymorphism in development of oral leukoplakia among tobacco users in North Indian population, this study was carried out at Department of Oral and Maxillofacial Pathology, King George's Medical University, Lucknow, UP. Study Design: Study include a total of 105 leukoplakia patients were genotyped for CYP2E1 polymorphism (93 males and 12 females; mean age ± SD: 47.5 ± 10.6) and 96 unrelated healthy controls (85 males and 11 females; mean age ± SD: 49 ± 11.1). All the patients had either reported for treatment of leukoplakia or were diagnosed with leukoplakia during routine oral examination. Results: A total of 105 leukoplakia patients and 96 controls were included in the study. The mean age of leukoplakia patients and control were 47 ± 10 and 51 ± 10 years respectively. The exclusive smokers comprised 62 (59%) leukoplakia patients and 53 (53%) controls. The exclusive smokeless tobacco users were 16 (15%) in leukoplakia patients and 27 (28%) in controls groups, while 27 (26%) leukoplakia patients and 16 (17%) controls have both types (smoking as well as smoke less) of tobacco habits simultaneously. Range of life time smoking exposure in leukoplakia and controls were (5-80 PY in both groups) but the mean smoking exposure in both groups were (leukoplakia: 28 ± 21.8 PY, control: 27: ±17 PY). But the mean smokeless tobacco dose in two groups were (leukoplakia: 150 ± 175 CY, controls: 137 ± 110 CY). Conclusion: All the results demonstrate an association between CYP2E1 genetic polymorphism and leukoplakia risk, premalignant lesion. It indicates that the CYP2E1 polymorphism, singly showed a protection towards the oral leukoplakia. Independent confirmation of this finding is required, and additional examination of the joint effect of CYP2E1genotype and other non-tobacco-related exposures is needed before more conclusive interpretation of our results can be made. This study demonstrates the importance of genetic variations in CYP2E1genes in susceptibility towards oral leukoplakia and it is conceivable that these variants will interact with environmental carcinogens and possibly some combinations of these genotypes will be at a high risk to oral leukoplakia.






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