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利用聚合酶链反应分析宫颈癌和正常宫颈上皮中16型人乳头瘤病毒E6-E7转录情况。

Analysis of human papillomavirus type 16 E6-E7 transcription in cervical carcinomas and normal cervical epithelium using the polymerase chain reaction.

作者信息

Johnson M A, Blomfield P I, Bevan I S, Woodman C B, Young L S

机构信息

Department of Cancer Studies, Cancer Research Campaign Laboratories, Birmingham, U.K.

出版信息

J Gen Virol. 1990 Jul;71 ( Pt 7):1473-9. doi: 10.1099/0022-1317-71-7-1473.

DOI:10.1099/0022-1317-71-7-1473
PMID:1695672
Abstract

Cervical biopsies were collected from Birmingham women having cervical intraepithelial neoplasia or invasive cervical carcinoma and normal controls, and examined for the presence of human papillomavirus type 16 (HPV-16) E6-E7 DNA and mRNA using an adaptation of the polymerase chain reaction. HPV-16 E6-E7 sequences were detected in all abnormal biopsies and in 90% of the normal biopsies examined, confirming previous studies describing the high prevalence of cervical HPV-16 infection. While we were unable to identify any qualitative differences in RNA transcripts from the p97 promoter, substantial quantitative differences in HPV-16-specific early region transcripts between normal and cytologically abnormal cervices were observed. These results suggest that although the level of E6-E7 transcription may contribute to the malignant phenotype, additional factors are likely to be important in the development of cervical neoplasia.

摘要

从患有宫颈上皮内瘤变或浸润性宫颈癌的伯明翰女性以及正常对照者中采集宫颈活检样本,采用改良的聚合酶链反应检测人乳头瘤病毒16型(HPV - 16)E6 - E7 DNA和mRNA的存在情况。在所有异常活检样本以及90%接受检测的正常活检样本中均检测到HPV - 16 E6 - E7序列,这证实了先前描述宫颈HPV - 16感染高患病率的研究。虽然我们无法确定来自p97启动子的RNA转录本存在任何定性差异,但在正常宫颈和细胞学异常宫颈之间观察到HPV - 16特异性早期区域转录本存在显著的定量差异。这些结果表明,尽管E6 - E7转录水平可能促成恶性表型,但其他因素在宫颈肿瘤形成过程中可能也很重要。

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Increased Ki-67 proliferative index and absence of P16INK4 in CIN-HPV related pathogenic pathways different from cervical squamous intraepithelial lesion.在与宫颈鳞状上皮内病变不同的CIN-HPV相关致病途径中,Ki-67增殖指数增加且P16INK4缺失。
Br J Ophthalmol. 2006 Jul;90(7):894-9. doi: 10.1136/bjo.2005.086314. Epub 2006 Mar 15.
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An AP-1 binding site mutation in HPV-16 LCR enhances E6/E7 promoter activity in human oral epithelial cells.
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Virus Genes. 2002;24(1):29-37. doi: 10.1023/a:1014081803232.
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