Publication: Codon72 polymorphism in the p53 tumor suppressor gene in oral lichen planus lesions in a Thai population
Issued Date
2010-01-01
Resource Type
ISSN
2476762X
15137368
15137368
Other identifier(s)
2-s2.0-78650683136
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Asian Pacific Journal of Cancer Prevention. Vol.11, No.4 (2010), 1137-1141
Suggested Citation
Pattamawadee Yanatatsaneeji, Nakarin Kitkumthorn, Chutintorn Dhammawipark, Jierada Rabalert, Vyomesh Patel, Apiwat Mutirangura Codon72 polymorphism in the p53 tumor suppressor gene in oral lichen planus lesions in a Thai population. Asian Pacific Journal of Cancer Prevention. Vol.11, No.4 (2010), 1137-1141. Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/28831
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Codon72 polymorphism in the p53 tumor suppressor gene in oral lichen planus lesions in a Thai population
Abstract
Background: Oral lichen planus (OLP) is a T-cell mediated autoimmune disease in which autocytotoxic CD8+ T cells (CTLs) trigger apoptosis of oral epithelial cells. Activated CTLs can produce Fas ligand and by binding to Fas lead to apoptosis. This Fas pathway and the action of p53 tumour suppressor gene are important in producing apoptosis. Current data demonstrate a link between these two factors at the transcriptional level. Objective: The purpose of this study was to investigate the p53 polymorphism at codon 72 which results in encoding of either proline or arginine. Methods: Our study used 97 OLP cases and 94 control blood samples from non-OLP individuals and performed PCR-RFLP. Results: Compared to control individuals, we found a significant increase in occurrence in OLP patients of the proline encoding cytosine allele (adjusted odd ratio (95% CI)=2.29 (1.42-3.70) and p=0.001). In addition, in individuals with the non-erosive type of OLP, the same situation was evident (OR=2.29, 95% CI (1.38-3.78), p=0.001). Furthermore, we noted a significantly higher prevalence of homozygosity [OR=3.17, 95% CI(1.58-7.25), p=0.001) for the p53 pro allele in the OLP group, which indicates a recessive mode of inheritance. Conclusion: Our data suggest a strong association between the pro/pro genotype and OLP, and that the process of apoptosis, in which p53 plays a role, is a factor in OLP pathogenesis.