Human papillomavirus (HPV) DNA sequences in oral precancerous lesions and squamous cell carcinoma demonstrated by in situ hybridization.
Human papillomavirus (HPV) DNA sequences in oral precancerous lesions and squamous cell carcinoma demonstrated by in situ hybridization.
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通过原位杂交证实口腔癌前病变和鳞状细胞癌中的人乳头瘤病毒 (HPV) DNA 序列。
DOI：
10.1111/j.1600-0714.1988.tb01536.x
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Happonen,RP
中科院分区：
文献类型：
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作者：
Syrjänen,SM;Syrjänen,KJ;Happonen,RP
首先使用原位DNA杂交技术，使用含有35 S标记的HPV 6、11、13、16、18和30型DNA的人乳头瘤病毒（HPV）DNA探针混合物，对73例手术治疗的口腔癌前病变（OPL）（22例）和口腔鳞状细胞癌（SCC）（51例）的一系列常规处理的石蜡包埋活检进行筛选。用原位杂交技术和6种HPV DNA探针对本实验中发现的HPV DNA进行了分型分析。总共12/73（16.4%）的病变被证明含有HPV DNA; 6/51（11.8%）的癌和6/21（28.6%）的发育不良。HPV DNA阳性病变最常见的部位是腭（4/7; 57%），其次是口底（2/8; 25%），舌和牙龈（11.8%）。HPV 13或HPV 30在所研究的任何病变中均未发现。HPV 11 DNA在2例轻度不典型增生中检出，而在癌中未检出.另外一个轻度异型增生被证明含有HPV 6 DNA。HPV 16 DNA在5例活检中检出，其中癌3例，不典型增生2例。在其中一个HPV 16阳性癌中，同时存在HPV 18 DNA。在另外3例癌和1例中度异型增生病变中仅发现HPV 18。结果证实了最近报道的HPV参与OPL和口腔癌的证据。这些研究结果的影响进行了讨论，在口腔鳞状细胞癌的可能的HPV病因。在常规处理的口腔活检研究中，原位DNA杂交作为一种强有力的工具（能够定位特定的HPV DNA序列并对同一部位的病变进行正确的分类）被强烈提倡。
A series of routinely processed, paraffin‐embedded biopsies from 73 surgically treated oral precancerous lesions (OPL) (22 cases), and oral squamous cell carcinomas (SCC) (51 cases), was first screened using an in situ DNA hybridization technique with a human papillomavirus (HPV) DNA probe cocktail containing the 35S‐labelled DNA of HPV types 6, 11, 13, 16, 18 and 30. The specific HPV types in lesions shown to contain HPV DNA in this procedure were further analysed by usingin situhybridization and the 6 HPV DNA probes separately. A total of 12/73 (16.4%) of the lesions proved to contain HPV DNA; 6/51 (11.8%) carcinomas and 6/21 (28.6%) dysplasias. The most frequent sites of HPV DNA‐positive lesions were palate (4/7; 57%), followed by the floor of the mouth (2/8; 25%), the tongue and gingiva (11.8%). HPV 13 or HPV 30 were not found in any of the lesions studied. HPV 11 DNA was demonstrated in 2 mild dysplasia lesions, but not in carcinomas. One additional mild dysplasia proved to contain HPV 6 DNA. HPV 16 DNA was present in 5 biopsies; 3 carcinomas and 2 dysplasias. In one of the HPV 16‐positive carcinomas, HPV 18 DNA was simultaneously present. HPV 18 alone was found in 3 additional carcinomas and in one moderate dysplasia lesion. The results confirm the recently reported evidence on HPV involvement in OPL and oral cancer. The implications of these findings are discussed in terms of the possible HPV etiology of oral SCC. The use of thein situDNA hybridization as a powerful tool (enabling the localization of specific HPV DNA sequences and the proper classification of the lesion at the same site) in the study of routinely processed oral biopsies is strongly advocated.