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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。
Objective: To study the relationship between the expression of p16, p5, Ki-67 and oral precancerous lesions. Methods: The expressions of p16, P53 and Ki-67 in 43 cases of epithelial dysplasia (20 mild epithelial dysplasia and 23 severe epithelial dysplasia) and 20 normal oral mucosa were detected by immunohistochemistry Conducted a study, and the actual rate of epithelial dysplasia in patients with a 4-year follow-up. Results: The normal mucosa group, p5 3 did not express, Ki-67 a small amount of expression, p16 positive expression was 10%. Mild epithelial dysplasia, p5 3, Ki-67 minority expression, p16 expression rate of 86.96%. Severe epithelial dysplasia, p5 3 and Ki-67 overexpression, p16 expression decreased significantly, compared with normal mucosa, mild epithelial dysplasia significant difference (P <0.05). The overexpression of p5 3 and Ki-67 protein and the low expression of p16 have some correlation with the actual cancerous rate of oral precancerous lesions. CONCLUSION: Oral mucosal carcinogenesis is a process from quantitative to qualitative change, and their regulatory genes p16, p5 3 and Ki -6 have significant changes and may play an important regulatory role.