ORAL-CANCER RISK IN RELATION TO SEXUAL HISTORY AND EVIDENCE OF HUMAN-PAPILLOMAVIRUS INFECTION

Citation
Sm. Schwartz et al., ORAL-CANCER RISK IN RELATION TO SEXUAL HISTORY AND EVIDENCE OF HUMAN-PAPILLOMAVIRUS INFECTION, Journal of the National Cancer Institute, 90(21), 1998, pp. 1626-1636
Citations number
58
Categorie Soggetti
Oncology
Volume
90
Issue
21
Year of publication
1998
Pages
1626 - 1636
Database
ISI
SICI code
Abstract
Background: Experimental models and analyses of human tumors suggest t hat oncogenic, sexually transmittable human papillomaviruses (HPVs) ar e etiologic factors in the development of oral squamous cell carcinoma (SCC), We conducted a population-based, case-control study to determi ne whether the risk of this cancer is related to HPV infection and sex ual history factors. Methods: Case subjects (n = 284) were 18-65-year- old residents of three counties in western Washington State who were n ewly diagnosed with oral SCC from 1990 through 1995. Control subjects (n = 477) similar in age and sex were selected from the general popula tion. Serum samples were tested for HPV type 16 capsid antibodies. Exf oliated 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 a lcohol consumption. Results: Among males only, oral SCC risk increased with self-reported decreasing age at first intercourse, increasing nu mber of sex partners, and a history of genital warts. Approximately 26 % of the tumors in case subjects contained HPV DNA; 16.5% of the tumor s contained HPV type 16 DNA, The prevalence of oncogenic HPV types in exfoliated oral tissue was similar in case and control subjects, The O Rs for HPV type 16 capsid seropositivity were 2.3 (95% confidence inte rval [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 cigare tte 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 in dividual 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 ty pe 16 infection may contribute to the development of a small proportio n of oral SCCs in this population, most likely in combination with cig arette smoking.