Antibodies to human papillomavirus 16 and subsequent in situ or invasive cancer of the cervix.

Antibodies to human papillomavirus 16 and subsequent in situ or invasive cancer of the cervix.
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DOI:
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发表时间:
1997-04
期刊:
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
影响因子:
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通讯作者:
K. Shah;R. Viscidi;A. Alberg;K. J. Helzlsouer;G. W. Comstock
K. Shah;R. Viscidi;A. Alberg;K. J. Helzlsouer;G. W. Comstock
中科院分区:
其他
文献类型:
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作者:
K. Shah;R. Viscidi;A. Alberg;K. J. Helzlsouer;G. W. Comstock

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我们的目的是检查过去感染人乳头瘤病毒 (HPV)-16(通过抗体测定确定)是否是后续宫颈癌的危险因素。 1975 年至 1990 年间,马里兰州华盛顿县的 11,000 多名健康女性中发生了原位或浸润性宫颈癌的病例。对 1974 年收集的病例和匹配对照的基线血清进行了检查,检测与 HPV-16(一种癌症相关 HPV)和 HPV-6(一种低危 HPV)病毒样颗粒有反应的 IgG 抗体。 11例诊断后血清也进行了类似评估。对 14 例浸润性宫颈癌、28 例原位宫颈癌和 83 例匹配对照进行了评估。主要结果指标是诊断前血清中含有 HPV-16 或 HPV-6 抗体的女性患宫颈癌的风险。 HPV-16 抗体而非 HPV-6 抗体是随后发生宫颈癌的标志。与匹配对照血清相比,病例血清与 HPV-16 病毒样颗粒的反应更频繁、更强烈。 HPV-16 抗体的存在与宫颈癌风险增加显着相关(比值比,3.9;95% 置信限,1.4,10.7);高 HPV-16 抗体水平与更高的宫颈癌风险相关(比值比 = 7.5,95% 置信限 1.5、36.3)。调整吸烟和受教育年限后,与宫颈癌的关联得到加强。在 11 对诊断前和诊断后血清的测试中,HPV-16 抗体在 7-13 年的时间内没有明显下降,并且 2 例病例似乎发生了 HPV-16 的血清转化。血清学数据表明,HPV-16 感染与未来患宫颈癌的风险相关,并加强了 HPV 在宫颈癌中病因学作用的证据。
Our objective was to examine whether past infection with human papillomavirus (HPV)-16, as determined by an antibody assay, is a risk factor for subsequent cervical cancer. Incident cases of in situ or invasive cervical cancer occurring between 1975 and 1990 in a cohort of over 11,000 healthy women in Washington County, MD, were identified. The baseline sera of cases and of matched controls, collected in 1974, were examined for IgG antibodies reactive with virus-like particles of HPV-16, a cancer-associated HPV, and HPV-6, a low-risk HPV. Postdiagnosis sera of 11 cases were also assessed similarly. Fourteen cases of invasive and 28 cases of in situ cervical cancer and 83 matched controls were evaluated. The main outcome measure was the risk of cervical cancer in women who had HPV-16 or HPV-6 antibodies in prediagnostic sera. Antibodies to HPV-16 but not to HPV-6 were a marker for subsequent occurrence of cervical cancer. Case sera were reactive more often and more strongly with HPV-16 virus-like particles than were sera of matched controls. The presence of antibodies to HPV-16 was significantly associated with an increased risk of cervical cancer (odds ratio, 3.9; 95% confidence limits, 1.4, 10.7); high antibody levels to HPV-16 were associated with an even greater risk of cervical cancer (odds ratio = 7.5, 95% confidence limits 1.5, 36.3). The association with cervical cancer was strengthened after adjustment for smoking and years of education. In tests of 11 pairs of pre- and postdiagnostic sera, HPV-16 antibodies did not decline markedly over a 7-13-year time period, and seroconversion to HPV-16 appeared to have occurred in 2 cases. The serological data indicate that HPV-16 infection is associated with future risk of cervical cancer and strengthen the evidence for the etiological role of HPVs in cervical cancer.