Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection
Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection
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DOI：
10.1093/jnci/90.21.1626
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发表时间：
1998-11-04
影响因子：
10.3
通讯作者：
Galloway, DA
中科院分区：
文献类型：
--
作者：
Schwartz, SM;Daling, JR;Galloway, DA
背景资料：实验模型和人类肿瘤的分析表明，致癌性，性传播的人乳头瘤病毒（HPV）是口腔鳞状细胞癌（SCC）的发病因素，我们进行了一项基于人群的病例对照研究，以确定这种癌症的风险是否与HPV感染和性史因素有关。研究方法：病例受试者（n = 284）为1990年至1995年新诊断为口腔鳞状细胞癌的华盛顿州西部三个县的18-65岁居民。从一般人群中选择年龄和性别相似的对照受试者（n = 477）。检测血清样品的HPV 16型衣壳抗体。从病例和对照受试者中收集的脱落口腔组织以及来自病例受试者的肿瘤组织进行HPV DNA检测。在校正年龄、性别、吸烟和饮酒后计算比值比（OR）。结果如下：仅在男性中，口腔鳞状细胞癌的风险随着自我报告的首次性交年龄的降低、性伴侣数量的增加和生殖器疣史而增加。病例中约26%的肿瘤含有HPV DNA; 16.5%的肿瘤含有HPV 16型DNA，在脱落的口腔组织中致癌HPV类型的患病率在病例和对照受试者中相似，HPV 16型衣壳血清阳性的OR为2.3（95%置信区间[CI] = 1.6-3.3），含HPV 16型DNA的口腔SCC为6.8（95% CI = 3.0-15.2）。吸烟和HPV 16型衣壳血清阳性与口腔鳞状细胞癌的联合相关性（OR = 8.5; 95%CI = 5.1-14.4）强于目前吸烟（OR = 3.2; 95%CI = 2.0-5.2）和血清阳性（OR = 1.7; 95%CI = 1.1-2.6）的个体相关性总和的预测。结论：HPV 16型感染可能导致该人群中小部分口腔SCC的发展，最有可能与吸烟相结合。
Background: Experimental models and analyses of human tumors suggest that oncogenic, sexually transmittable human papillomaviruses (HPVs) are etiologic factors in the development of oral squamous cell carcinoma (SCC), We conducted a population-based, case-control study to determine whether the risk of this cancer is related to HPV infection and sexual history factors. Methods: Case subjects (n = 284) were 18-65-year-old residents of three counties in western Washington State who were newly diagnosed with oral SCC from 1990 through 1995. Control subjects (n = 477) similar in age and sex were selected from the general population. Serum samples were tested for HPV type 16 capsid antibodies. Exfoliated oral tissue collected from case and control subjects and tumor tissue from case subjects were tested for HPV DNA. Odds ratios (ORs) were calculated after adjusting for age, sex, cigarette smoking, and alcohol consumption. Results: Among males only, oral SCC risk increased with self-reported decreasing age at first intercourse, increasing number of sex partners, and a history of genital warts. Approximately 26% of the tumors in case subjects contained HPV DNA; 16.5% of the tumors contained HPV type 16 DNA, The prevalence of oncogenic HPV types in exfoliated oral tissue was similar in case and control subjects, The ORs for HPV type 16 capsid seropositivity were 2.3 (95% confidence interval [CI] = 1.6-3.3) for all oral SCCs and 6.8 (95% CI = 3.0-15.2) for oral SCCs containing HPV type 16 DNA. The joint association of cigarette smoking and HPV type 16 capsid seropositivity with oral SCC (OR = 8.5; 95% CI = 5.1-14.4) was stronger than predicted from the sum of individual associations with current smoking (OR = 3.2; 95% CI = 2.0-5.2) and seropositivity (OR = 1.7; 95% CI = 1.1-2.6). Conclusions: HPV type 16 infection may contribute to the development of a small proportion of oral SCCs in this population, most likely in combination with cigarette smoking.