论文部分内容阅读
目的 探讨食管癌高发区中人乳头瘤病毒 (HPV)、爱泼斯坦 巴尔病毒 (EBV)与食管癌发病的关系 ,并初步研究HPV感染与p5 3过表达之间的关系。方法 设计了多对引物进行PCR、原位杂交及原位PCR、免疫组化 ,并对 30例高发区食管癌进行检测。结果 用PCR检出HPV L1阳性率10 .0 % ,HPV 16 E6阳性率 6 0 .0 % ,HPV 16 E7阳性率 6 3.3% ,HPV 18 E6及EBV的检出率分别为 6 .7%和 0 ,p5 3蛋白的检出率为 73.3%。用原位杂交和原位PCR检出HPV 16 E6阳性率均为 5 3.3%。HPV L1的低检出率及HPV 16 E6、HPV 16 E7基因的较高检出率可能提示 ,在肿瘤细胞中HPV常以部分丢失的形式整合 ,而E6、E7常在整合中保留。结论 HPV 16型可能与高发区食管癌发生密切相关 ,而HPV 18、EBV则关系不大。p5 3突变在食管癌的发病中起重要作用 ,但其与HPV感染之间的关系不大。
Objective To investigate the relationship between human papillomavirus (HPV), Epstein-Barr virus (EBV) and esophageal cancer in the high incidence area of esophageal cancer, and to study the relationship between HPV infection and p53 overexpression. Methods Multiple pairs of primers were designed for PCR, in situ hybridization, in situ PCR and immunohistochemistry. Esophageal cancer was detected in 30 high-risk areas. Results The positive rate of HPV L1 was 10.0%, the positive rate of HPV 16 E6 was 60%, the positive rate of HPV 16 E7 was 63.3%, and the detection rate of HPV 18 E6 and EBV was 6.7%. The detection rate of 0, p53 protein was 73.3%. The positive rate of HPV 16 E6 detected by in situ hybridization and in situ PCR was 5 3.3%. The low detection rate of HPV L1 and the higher detection rate of HPV 16 E6 and HPV 16 E7 genes may suggest that HPV often integrates in the form of partial loss in tumor cells, while E6 and E7 often remain in the integration. Conclusion HPV type 16 may be closely related to the occurrence of esophageal cancer in high-risk areas, while HPV 18 and EBV are not significantly related. The p53 mutation plays an important role in the pathogenesis of esophageal cancer, but its relationship with HPV infection is not significant.