| 张伟,金顺钱,刘伯奇,梁肖,商铭,孙建衡,吴爱如,王希霞,章文华,黎均跃.人乳头瘤病毒感染与发生宫颈癌及非癌宫颈疾患危险性分析[J].Chinese journal of Epidemiology,1993,14(5):300-303 |
| 人乳头瘤病毒感染与发生宫颈癌及非癌宫颈疾患危险性分析 |
| Relative Risk Analysis of the Development of Cervical Noncancer Lesion and Cervical Carcinoma Associated with HPV Infection |
| Received:January 28, 1993 Revised:May 08, 1993 |
| DOI： |
| KeyWord: 人乳头瘤病毒 宫颈癌 相对危险性 斑点杂交 |
| English Key Word: Papillomaviruses Cervical cancer Relative risk Dot blot hybridization |
| FundProject: |
| Author Name | Affiliation | | Zhang Wei | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 金顺钱 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 刘伯奇 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 梁肖 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 商铭 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 孙建衡 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 吴爱如 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 王希霞 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 章文华 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 | | 黎均跃 | Cancer Institute, Chines Academy of Medical Sciences, Beijing 100021 |
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| Abstract: |
| 采用斑点杂交技术对247份宫颈癌、143份非癌宫颈疾患活检组织标本分别进行了人乳头瘤病毒6/11(HPV6/11)、HPV16和18型DNA序列检测,实验结果指出:(1)247份宫颈癌标本中,HPV同源序列检出率为65.99%,其中HPV16型检出率为55.06%,占全部宫颈癌HPV阳性标本的71.28%,分别为该组HPV6/11及18型感染的4.25倍和5.67倍。(2)143例非癌宫颈疾患标本中,HPV检出率为51.05%,其中HPV6/11型占全部阳性标本的50.61%。(3)分析比较非癌宫颈疾患组与宫颈癌组HPV感染与宫颈癌发生的危险性,发现HPV感染后发生宫颈癌危险性明显增高(RR=1.86, P<0.01);比较两组HPV16/18感染,发现HPV16/18型感染后宫颈癌发生的危险进一步增加(RR=3.43, P<0.001);比较两组6/11感染与宫颈癌发生无关。以上结果提示与非癌宫颈疾患相比,宫颈癌的发生可能与HPV感染有关,尤其与HPV16/18型感染关系最为密切。 |
| English Abstract: |
| Two-hundred and fourty-seven DNA samples extracted from cervical carcinoma tissuses and 143 from cervical noncancer lesions were examined for the presence of human papillomavirus (HPV) type 6B, 11, 16 and 18 DNA sequences by means of dot blot hybridization using 32P-dCTP-labelled HPV probes (Tm-17℃). The result showed that the overall positive rate of HPV infection in this group of cervical cancer was 65.99%, HPV type 16 was dominantly found in the group (55.06%) and accounted for 71.28% in all the positive samples of cervical cancers, which were 4.25 and 5.67 times higher than those of HPV type 6/11 and 18, respectively. Detectable sequences homologous to HPVs in the cervical noncancer group was 51.05% and HPV types 6/11 accounted for 50.61% in the HPV-positive samples. The relative risk analysis of HPV infection in the two groups was performed and the relative risk (RR) of HPV infection for development of cervical cancer was increased (RR=1.86, P<0.01). Futher analysis revealed that HPV 16, 18 infection in cervical epithelium might be the higher risk factor in the development of cervical carcinoma (RR=3.43, P<0.001); whereas HPV type 6/11 might be the lower risk factor for the development of cervical cancer (RR=0.5, P<0.05). Our results implied that the development of cervical cancer may be closely associated with HPV infection, especially with HPV type 16 and 18. |
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