Correlation of HPV16E6 with p53 in oral cancer

龙小佳; 何力; 王璐; 邱丽华; 吴小红

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Correlation of HPV16E6 with p53 in oral cancer

更新时间：2026-01-09

- Correlation of HPV16E6 with p53 in oral cancer
- Journal of Army Medical University Vol. 38, Issue 21, Pages: 2326-2329(2016)
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  CLC： R394.2;R730.23;R739.8
- Published：2016
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龙小佳,何力,王璐,邱丽华,吴小红.HPV16E6和p53在口腔癌中的表达及相关性研究[J].陆军军医大学学报(原第三军医大学学报),2016,38(21):2326-2329.

　Long Xiaojia,He Li,Wang Lu,Qiu Lihua,Wu Xiaohong.Correlation of HPV16E6 with p53 in oral cancer[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(21):2326-2329.
龙小佳,何力,王璐,邱丽华,吴小红.HPV16E6和p53在口腔癌中的表达及相关性研究[J].陆军军医大学学报(原第三军医大学学报),2016,38(21):2326-2329. DOI：

　Long Xiaojia,He Li,Wang Lu,Qiu Lihua,Wu Xiaohong.Correlation of HPV16E6 with p53 in oral cancer[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(21):2326-2329. DOI：

摘要

目的探讨HPV16E6和抑癌基因p53在口腔癌中的表达，及其与口腔癌临床分期、病理分级的相关性。方法用免疫组织化学方法检测149例口腔癌、88例口腔癌癌前病变和49例癌周正常组织标本中HPV16E6和p53的表达，统计口腔癌不同临床分期和病理分级中HPV16E6和p53的阳性表达率。结果口腔癌组织、口腔癌癌前病变组织和口腔癌癌周正常组织中HPV16E6的阳性表达率分别为79.9%(119/149)、38.6%(34/88)和2.0%(1/49)，p53的阳性表达率分别为24.2%(36/149)、55.7%(49/88)和91.8%(45/49)。随着临床分期和病理分级的增加，HPV16E6阳性表达率明显增加，而p53阳性表达率却明显减少（P0.05）。结论 HPV16E6蛋白的表达升高和p53蛋白的表达降低可能会导致口腔癌的发生和发展。检测患者口腔癌组织中HPV16E6和p53的表达可用于评定口腔癌的恶性程度。

Abstract

Objective To investigate the expression of human papillomavirus type 16 E6 (HPV16E6) and p53 in human oral cancer and their relationship with clinical stage and histopathological grade. Methods Expression of HPV16E6 and p53 was detected by immunohistochemical staining in 149 oral cancer specimens

88 precarcinoma tissues and 49 normal oral tissues. Statistical analysis was performed on the positive expression of HPV16E6 and p53 with different clinical stages and histopathological grades. Results The positive rates of HPV16E6 were 79.9% (119/149) in oral cancer tissues

38.6% (34/88) in precarcinoma tissues and 2.0% (1/49) in normal oral tissues

respectively. The positive rates of p53 were 24.2% (36/149) in oral cancer tissues

55.7% (49/88) in precarcinoma tissues and 91.8% (45/49) in normal tissues

respectively. In parallel with the increases of clinical stage and histopathological grade

the positive rates of HPV16E6 were gradually increased

whereas those of p53 were gradually decreased (P0.05). Conclusion Up-regulation of HPV16E6 and down-regulation of p53 may contribute to the genesis of human oral cancer. Detection of HPV16E6 and p53 expression may be useful to evaluate the malignancy of oral cancer.

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