COFACTORS WITH HUMAN-PAPILLOMAVIRUS IN A POPULATION-BASED STUDY OF VULVAR CANCER

Background: Human papillomavirus (HPV) has been previously associated with vulvar cancer, In a population-based study, we examined whether e xposure to HPV, cigarette smoking, or herpes simplex virus 2 (HSV2) in creases the risk of this cancer, Methods: Incident cases of in situ (n = 400) and invasive (n = 110) squamous cell vulvar cancer diagnosed a mong women living in the Seattle area from 1980 through 1994 were iden tified. Serum samples were analyzed for antibodies against specific HP V types and HSV2, HPV DNA in tumor tissue was detected by means of the polymerase chain reaction, In most analyses, case subjects were compa red with population-based control subjects (n = 1403). Relative risks of developing vulvar cancer were estimated by use of adjusted odds rat ios (ORs) and 95% confidence intervals (CIs), Results: Increased risks of in situ or invasive vulvar cancer were associated with HPV16 serop ositivity (ORs = 3.6 [95% CI = 2.6-4.8] and 2.8 [95% CI = 1.7-4.7], re spectively), current cigarette smoking (ORs = 6.4 [95 % CI = 4.4-9.3] and 3.0 [95% CI = 1.7-5.3], respectively), and HSV2 seropositivity (OR s = 1.9 [95% CI = 1.4-2.6] and 1.5 [95% CI = 0.9-2.6], respectively), When the analysis was restricted to HPV16 DNA-positive tumors (in situ or invasive), the OR associated with HPV16 seropositivity was 4.5 (95 % CI = 3.0-6.8), The OR for vulvar cancer was 18.8 (95% CI = 11.9-29.8 ) among current smokers who were HPV16 seropositive in comparison with never smokers who were HPV16 seronegative. Conclusions: Current smoki ng, infection with HPV16, and infection with HSV2 are risk factors for vulvar cancer. Risk appears particularly strong among women who are b oth current smokers and HPV16 seropositive.