摘要
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 association of HPV with the development of esophageal cancer(EC) in a high incidence area of EC and to elucidate its correlation with p53 overexpression.Methods Thirty EC specimeas were collected from Anyang, Henan. Four pairs of primers were designed to perform in situ hybridization (ISH)and in situ PCR(ISPCR). Immunohistochemical staining was used to detect p53.Results HPV L1, HPV 16 E6 and HPV 16 E7 was detected in 10.0%,60.0% and 63.3% of the EC samples, respectively. The detection rate of HPV 18 E6 was low(6.7%) and no EBV was detected. Overexpression of p53 was identified in 73.3% EC. With ISH or ISPCR, HPV 16 E6 was positive in 53.3% of EC. Conclusion The low detection rate of HPV L1 and high detection rate of HPV 16 E6 and E7 genes suggest that HPV may be partially lost when inte grating into tumor cell genome,while E6 and E7 genes are intact. The results support a role of HPV 16 in the pathogenesis of EC in high incidence area. Although p53 mutation takes an important part in tumor pathogenesis, it is not consistent with the HPV existence in the EC cells.
出处
《中华肿瘤杂志》
CAS
CSCD
北大核心
2001年第3期220-223,共4页
Chinese Journal of Oncology
基金
国家自然科学基金资助项目(30070834)
关键词
食管肿瘤
人乳头瘤病毒
P53基因
原位杂交
聚合酶链反应
Esophageal neoplasms
Human papillomavirus
p53 gene
In situ hybridization
Polymerase chain reaction
