p16,p53,Ki67在口腔癌前病变表达及4年临床随访

目的 :研究 p16,p5 3 ,Ki-67蛋白表达与口腔癌前病变的关系。 方法 :采用免疫组织化学LsAB法对43例上皮异常增生 ( 2 0例轻度上皮异常增生 ,2 3例重度上皮异常增生 )和 2 0例正常口腔黏膜 p16,P5 3和Ki -67蛋白的表达进行研究 ,并对上皮异常增生患者实际癌变率做了 4年追踪。结果 :正常黏膜组 ,p5 3不表达 ,Ki -67少量表达 ,p16的阳性表达为 10 0 %。轻度上皮异常增生 ,p5 3 ,Ki-67少数表达 ,p16表达率为 86.96%。重度上皮异常增生 ,p5 3和Ki-67过度表达 ,p16表达明显下降 ,与正常黏膜 ,轻度上皮异常增生相比差异显著 (P <0 .0 5 )。p5 3和Ki-67蛋白过度表达而 p16呈低表达与实际口腔癌前病变癌变率有一定相关性。 结论 :口腔黏膜癌变是一个由量变到质变的过程 ,它们的调控基因 p16,p5 3 ,Ki -6发生了显著的变化 ,可能起着重要的调控作用。

The expression of p16, p53 and Ki-67 protein in epithelial dysplasia from oral mucosa and a follow-up study of four years

Objective:To study the relationship between the malignant transformation of oral epithelial dysplasia and the expression of p16, p53 and Ki-67 proteins.Method:The expression of p16, p53 and Ki-67 proteins was determined from 43 cases of oral epithelial dysplasia and 20 normal oral mucosa tissue by immunihistochemistry,and a follow-up study of four years was made.Result:In normal epithelium, Ki-67 express was only observed in a small number of cells, and no expression of p53, p16 expression was 100%. In mild epithelial dysplasia, Ki-67 and p53 had low express, express rate of p16 was 86.96%. In sever epithelial dysplasia, there were a number of positive cell of p53 and Ki-67, expression of p16 was significantly decreased.there is a co-relationship between the malignant transformation and mutation of p53 ,ki-67 and p16 in the cases of oral epithelial dysplasia.Conclusion: Carcinogenesis of oral mucosa is a continuous and stepwise course, p16, p53, Ki-67 genes may play an important role in this course. .