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泰国人群口腔扁平苔藓病变中p53肿瘤抑制基因的密码子72多态性

Codon72 polymorphism in the p53 tumor suppressor gene in oral lichen planus lesions in a Thai population.

作者信息

Yanatatsaneeji Pattamawadee, Kitkumthorn Nakarin, Dhammawipark Chutintorn, Rabalert Jierada, Patel Vyomesh, Mutirangura Apiwat

机构信息

Department of Botany, Faculty of Science, Chulalongkorn University, Bangkok, Thailand.

出版信息

Asian Pac J Cancer Prev. 2010;11(4):1137-41.

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.

摘要

背景

口腔扁平苔藓(OLP)是一种T细胞介导的自身免疫性疾病,其中自身细胞毒性CD8 + T细胞(CTL)触发口腔上皮细胞凋亡。活化的CTL可产生Fas配体,并通过与Fas结合导致凋亡。这种Fas途径和p53肿瘤抑制基因的作用在产生凋亡中很重要。目前的数据表明这两个因素在转录水平上存在联系。

目的

本研究的目的是调查第72密码子处的p53多态性,该多态性导致脯氨酸或精氨酸的编码。

方法

我们的研究使用了97例OLP病例和94例来自非OLP个体的对照血样,并进行了PCR-RFLP。

结果

与对照个体相比,我们发现OLP患者中编码脯氨酸的胞嘧啶等位基因的发生率显著增加(调整后的优势比(95%CI)= 2.29(1.42 - 3.70),p = 0.001)。此外,在非糜烂型OLP个体中,同样的情况很明显(OR = 2.29,95%CI(1.38 - 3.78),p = 0.001)。此外,我们注意到OLP组中p53脯氨酸等位基因的纯合子患病率显著更高[OR = 3.17,95%CI(1.58 - 7.25),p = 0.001],这表明是隐性遗传模式。

结论

我们的数据表明pro / pro基因型与OLP之间存在强烈关联,并且p53起作用的凋亡过程是OLP发病机制中的一个因素。

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