"High risk" HPV types are frequently detected in potentially malignant and malignant oral lesions, but not in normal oral mucosa
"High risk" HPV types are frequently detected in potentially malignant and malignant oral lesions, but not in normal oral mucosa
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DOI：
10.1038/modpathol.3880113
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发表时间：
2000-06-01
期刊：
影响因子：
7.5
通讯作者：
Kittas, C
中科院分区：
文献类型：
--
作者：
Bouda, M;Gorgoulis, VG;Kittas, C
关于人乳头瘤病毒（HPV）参与口腔肿瘤发生和发展的研究产生了相互矛盾的结果。观察到的差异主要是由于不同的敏感性的应用方法和流行病学因素的检查患者群体。为了评估HPV在口腔癌发生中的作用，我们分析了53个潜在的肿瘤和肿瘤性口腔病变，包括29例增生，5例异型增生，19例鳞状细胞癌，以及16个来自健康个体的口腔标本。一个高灵敏度的巢式聚合酶链反应（PCR）检测，沿着类型特异性PCR，限制性片段长度多态性分析，斑点印迹，和非同位素原位杂交。巢式PCR显示HPV DNA的存在，在48（91%）的53个病理样本分析，而没有（0%）的正常标本被发现感染。HPV阳性与分析组患者的组织学和吸烟习惯无关。在47例（98%）感染标本中通过类型特异性PCR检测到至少一种“高危”类型，如HPV 16、18和33，而只有1例（2%）鳞状细胞癌仅感染“低危”类型（HPV 6）。HPV 16是流行的病毒类型，存在于71%的感染病例中。经限制性片段长度多态性分析证实为单一的HPV16和HPV18感染。3例增生性病变用斑点杂交法检测HPV58。HPV阳性和基因分型得到进一步证实，这种病毒的物理状态进行了评价，通过非同位素原位杂交。低危型和高危型分别观察到弥漫性和点状信号，表明HPV感染的游离型和整合型。我们的研究结果提示高危型HPV早期参与口腔癌的发生。
Studies on the involvement of the human papillomavirus (HPV) in initiation and progression of oral neoplasia have generated conflicting results. The observed discrepancy is attributable mainly to the varying sensitivity of the applied methodologies and to epidemiologic factors of the examined patient groups. To evaluate the role of HPV in oral carcinogenesis, we analyzed 53 potentially neoplastic and neoplastic oral lesions consisting of 29 cases of hyperplasia, 5 cases of dysplasia, and 19 cases of squamous cell carcinomas, as well as 16 oral specimens derived from healthy individuals. A highly sensitive nested polymerase chain reaction (PCR) assay was used, along with type-specific PCR, restriction fragment length polymorphism analysis, dot blotting, and nonisotopic in situ hybridization. Nested PCR revealed the presence of HPV DNA in 48 of the 53 (91%) pathologic samples analyzed, whereas none (0%) of the normal specimens was found to be infected. Positivity for HPV was independent of histology and the smoking habits of the analyzed group of patients. At least one "high risk" type, such as HPV 16, 18, and 33, was detected by type-specific PCR in 47 (98%) infected specimens, whereas only 1 (2%) squamous cell carcinoma was solely infected by a "low risk" type (HPV 6). HPV 16 was the prevailing viral type, being present in 71% of infected cases. Single HPV 16 and HPV 18 infections were confirmed by restriction fragment length polymorphism. HPV 58 was detected by dot blotting in three hyperplastic lesions. HPV positivity and genotyping were further confirmed, and the physical status of this virus was evaluated by nonisotopic in situ hybridization. Diffuse and punctate signals, indicative of the episomal and integrative pattern of HPV infection, were observed for low- and high-risk types, respectively. Our findings are suggestive of an early involvement of high-risk HPV types in oral carcinogenesis.