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正常、潜在恶性及恶性口腔黏膜中的人单纯疱疹病毒1型和16型乳头瘤病毒同源DNA序列

Human herpes simplex-1 and papillomavirus type 16 homologous DNA sequences in normal, potentially malignant and malignant oral mucosa.

作者信息

Cox M, Maitland N, Scully C

机构信息

Centre for the Study of Oral Disease, University Department of Oral Medicine, Bristol Dental Hospital and School, UK.

出版信息

Eur J Cancer B Oral Oncol. 1993 Jul;29B(3):215-9. doi: 10.1016/0964-1955(93)90025-a.

DOI:10.1016/0964-1955(93)90025-a
PMID:8298425
Abstract

We have tested a range of normal, potentially malignant and malignant oral mucosal biopsies tissues by Southern blot hybridisation analysis for the simultaneous presence of HSV-1 and HPV type 16 DNA sequences, both of which have been implicated as risk factors in oral carcinogenesis. The results show that: (1) 2/4 patients with lichen planus, 2/4 patients with non-specific keratosis, 1/8 patients with oral carcinoma and 3/5 biopsy specimens of normal oral mucosa contained DNA sequences homologous to the HSV-1, Bam HI-G fragment. (2) HPV-16 homologous DNA sequences were detected in 3/4 patients with lichen planus, 4/4 non-specific keratosis, 4/8 oral carcinomas and in 3/5 biopsy specimens of normal oral mucosa. (3) Overall, only 5 patient biopsy specimens were positive for both HSV-1 and HPV-16 homologous DNA sequences; 2 lichen planus, 2 non-specific keratosis and 1 normal. The data cannot exclude a "hit and run" oncogenic mechanism for HSV but suggest that if HSV-1 and HPV-16 play a synergistic role in the development of oral cancer this may be an early event. Indeed, the data suggest HSV might be more frequently found in potentially malignant lesions than in carcinoma.

摘要

我们通过Southern印迹杂交分析对一系列正常、潜在恶性和恶性口腔黏膜活检组织进行了检测,以同时检测单纯疱疹病毒1型(HSV-1)和16型人乳头瘤病毒(HPV-16)的DNA序列,这两种病毒均被认为是口腔癌发生的危险因素。结果显示:(1)4例扁平苔藓患者中有2例、4例非特异性角化病患者中有2例、8例口腔癌患者中有1例以及5例正常口腔黏膜活检标本中有3例含有与HSV-1 Bam HI-G片段同源的DNA序列。(2)在4例扁平苔藓患者中有3例、4例非特异性角化病患者中有4例、8例口腔癌患者中有4例以及5例正常口腔黏膜活检标本中有3例检测到HPV-16同源DNA序列。(3)总体而言,仅5例患者活检标本的HSV-1和HPV-16同源DNA序列均为阳性;2例扁平苔藓、2例非特异性角化病和1例正常标本。这些数据不能排除HSV的“打了就跑”致癌机制,但表明如果HSV-1和HPV-16在口腔癌发生中起协同作用,这可能是一个早期事件。实际上,数据表明HSV在潜在恶性病变中比在癌中更常见。

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