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宫颈上皮内肿瘤(CIN)的克隆性状态与HPV感染的关系

Relationship between the clonality status of cervical intraepithelial neoplasm and HPV infection
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摘要 目的:应用原位杂交方法检测不同克隆性状态的宫颈上皮内肿瘤(CIN)内人乳头状瘤病毒(HPV)感染率以及类型,探讨不同克隆性状态的CIN与HPV感染的关系,明确HPV(特别是高危型HPV)在单克隆性增生CIN和宫颈癌发生、发展中的作用。方法:采用原位杂交方法检测24例CINⅠ标本(2例单克隆性增生、22例多克隆性增生)、20例CINⅡ标本(13例单克隆性增生、7例多克隆性增生)、19例CINⅢ标本(均为单克隆性增生)HPV16/18、HPV6/11的表达状况。结果:34例单克隆性增生CIN中HPV16/18的阳性表达率为58.8%(20/34),HPV6/11的阳性表达率为26.5%(9/34),两者均为阳性5.9%(2/34),两者均为阴性20.6%(7/34);29例多克隆性增生CIN中HPV16/18的阳性表达率为10.3%(3/29),HPV6/11的阳性表达率为24.2%(7/29),两者均为阳性6.9%(2/29),两者均为阴性72.4%(21/29)。结论:单克隆性增生CINHPV16/18感染率明显高于多克隆性增生CIN(P<0.01)。HPV16/18感染是诱发单克隆性增生CIN重要因素。HPV16/18可能通过引起宫颈鳞状上皮的克隆性增生,促进细胞的转化和增殖,导致CIN的发生,并最终引起宫颈癌的发生、发展。 Objective:To investigate the relationship between cervical intraepithelial neoplasm (CIN) of different clonality status and HPV infection and identify the role of HPV(especially of high risk HPV) in monoclonal proliferative CIN and cervical carcinoma (CC) by detecting the infection rate and the types of HPV in CIN of different clonality status by in situ hybridization. Methods: To detect the expression status of HPV16/18, HPV6/11 by in situ hybridization in 24 samples of CIN I( 2 samples of monoclonal proliferation, 22 samples of polyclonal proliferation), 20 samples of CIN II( 13 samples of monoclonal proliferation, 7 samples of polyclonal proliferation), and 19 samples of CIN III (all samples were of monoclonal proliferation). Results: In 34 monoclonal proliferative CIN cases, the positive expression rate of HPV 16/18 was 58. 8% (20/34) ,the positive expression rate of HPV 6/11 was 26.5% (9/34), the positive rate of both HPV 16/18 and HPV 6/11 was 5.9% (2/34), the negative rate of both HPV 16/18 and HPV 6/11 was 20.6% (7/34) ; In 29 polyclonal proliferative CIN cases, the rate was 10.3% (3/29), 24.2% (7/29), 6.9% (2/29), 72.4% (21/29), respectively. Conclusion : HPV 16/18 infection rates of monoclonal proliferation in CIN were significantly higher than polyclonal lesions. HPV 16/18 infection is an important factor inducing monoclonal proliferative CIN. By causing the clonal proliferation of cervical squamous epithelium, HPV 16/18 promote cell transformation and proliferation, and ultimately cause the genesis and development of cervical carcinoma.
出处 《现代肿瘤医学》 CAS 2007年第12期1819-1823,共5页 Journal of Modern Oncology
基金 国家自然科学基金资助项目(No.30171052) 国家回国人员研究启动基金资助项目(Hg98004) 陕西省卫生厅科研基金资助项目(02D02)
关键词 宫颈上皮内肿瘤 宫颈癌 人乳头状瘤病毒 原位杂交 cervical intraepithelial neoplasm cervical carcinoma HPV in situ hybridization
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  • 1Busque L,Blood,1996年,88卷,1期,59页
  • 2Tsao S,Gynecol Oncol,1993年,48卷,1期,5页
  • 3Hendriks R W,Human Mol Genet,1992年,1卷,3期,187页
  • 4Singer Sam J,Gene,1984年,32卷,3期,409页
  • 5Liu Q,Establishment PCR based PGK clonality analysis,2000年
  • 6Ren D H,Surgicalpathology(第2版),1999年,793页
  • 7Zehbe I, Voglino G, Wilander E, et al. P53 codon 72 polymorphism and various human papillomavirus 16E6 genotypes are risk factors for cervical cancer development[J].Cancer Res,2001, 61(2):608-611.
  • 8Humbey O, Aubin F, Cairey-Remommay S, et al. TP53 polymorphism at exon 4 in Caucasian women from eastern France:lack of correlation with HPV status and grade of cervical precancerous lesions[J].Eur J Obstet Gynecol Repro Bio, 2002, 103(1):60-64.
  • 9Carico E, Atlante M, Bucci B, et al. E-cadherin and alpha-catenin expression during tumor progression of cervical carcinoma[J].Gynecol Oncol, 2001, 80(2):156-161.
  • 10Beckman G, Birgander R, Sjalander A, et al. Is P53 polymorphism maintained by natural selection[J]?Hum Hered, 1994, 44(5):266-270.

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