Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection

被引:422
作者
Schwartz, SM
Daling, JR
Doody, DR
Wipf, GC
Carter, JJ
Madeleine, MM
Mao, EJ
Fitzgibbons, ED
Huang, SX
Beckmann, AM
McDougall, JK
Galloway, DA
机构
[1] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98109 USA
[2] Univ Washington, Sch Publ Hlth & Community Med, Dept Epidemiol, Seattle, WA 98195 USA
[3] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Canc Biol, Seattle, WA 98109 USA
[4] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA
[5] Univ Washington, Sch Med, Dept Microbiol, Seattle, WA 98195 USA
来源
JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE | 1998年 / 90卷 / 21期
关键词
D O I
10.1093/jnci/90.21.1626
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
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收藏
页码:1626 / 1636
页数:11
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