Lorincz A T, Temple G F, Kurman R J, Jenson A B, Lancaster W D
Department of Molecular Diagnostics, Bethesda Research Laboratories, Life Technologies, Inc., Gaithersburg, MD 20877.
J Natl Cancer Inst. 1987 Oct;79(4):671-7.
Molecular hybridization analysis of human papillomavirus (HPV) DNA from 190 cervical biopsy specimens from women in the United States, Brazil, and Peru revealed viral sequences in 2 (9%) of 23 biopsy specimens of normal mature squamous epithelium, 7 (44%) of 16 biopsy specimens of metaplastic squamous epithelia, 60 (77%) of 78 cervical intraepithelial neoplasia (CIN), 57 (89%) of 64 invasive squamous carcinomas, and 8 (89%) of 9 endocervical adenocarcinomas. HPV typing by DNA hybridization revealed HPV 6 and HPV 11 sequences in metaplastic squamous epithelia, CIN I, and CIN II, but not in CIN III lesions or invasive carcinomas. HPV 16 was detected in metaplastic epithelium and in nearly half of the invasive squamous carcinomas and adenocarcinomas. It was present in 31% of CIN lesions, increasing in frequency with the severity of CIN from 20% of CIN I to 50% of CIN III. HPV 16 showed a striking difference in geographic distribution, being detected in 36% of the carcinomas from the United States compared to 64% of the carcinomas from Brazil and Peru. HPV 18 was found in metaplastic epithelia and in 17% of carcinomas but in only 1% of CIN lesions. HPV 31 was not found in metaplastic epithelium but was present in 6% of carcinomas and in 18% of CIN lesions. In addition, a group of uncharacterized HPVs, not corresponding to any of the probes used, was found in 5% of normal and metaplastic epithelia and in 18% of CIN and 19% of invasive cancers. These results suggest that individual HPV types that infect the cervix have varying degrees of oncogenic association. HPV 6 and HPV 11 appear to have very little oncogenic association, HPV 31 has low oncogenic association, and HPV 16 and HPV 18 have high oncogenic association.
对来自美国、巴西和秘鲁女性的190份宫颈活检标本进行人乳头瘤病毒(HPV)DNA分子杂交分析,结果显示,在23份正常成熟鳞状上皮活检标本中有2份(9%)检测到病毒序列,16份化生鳞状上皮活检标本中有7份(44%)检测到病毒序列,78份宫颈上皮内瘤变(CIN)中有60份(77%)检测到病毒序列,64份浸润性鳞状细胞癌中有57份(89%)检测到病毒序列,9份宫颈管腺癌中有8份(89%)检测到病毒序列。通过DNA杂交进行HPV分型显示,在化生鳞状上皮、CIN I和CIN II中检测到HPV 6和HPV 11序列,但在CIN III病变或浸润性癌中未检测到。在化生上皮以及近一半的浸润性鳞状细胞癌和腺癌中检测到HPV 16。它存在于31%的CIN病变中,随着CIN严重程度的增加,其频率从CIN I的20%增加到CIN III的50%。HPV 16在地理分布上存在显著差异,在美国36%的癌症中检测到,而在巴西和秘鲁64%的癌症中检测到。在化生上皮以及17% 的癌症中发现了HPV 18,但仅在1% 的CIN病变中发现。在化生上皮中未发现HPV 31,但在6% 的癌症和18% 的CIN病变中存在。此外,在5% 的正常和化生上皮、18% 的CIN以及19% 的浸润性癌中发现了一组未鉴定的HPV,它们与所使用的任何探针均不对应。这些结果表明,感染宫颈的个体HPV类型具有不同程度 的致癌关联。HPV 6和HPV 11似乎几乎没有致癌关联,HPV 31致癌关联较低,而HPV 16和HPV 18致癌关联较高。