title: Oral cancer risk in relation to sexual history and evidence of human papillomavirus infection.
abstract: 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.
authors.affiliation: Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA.
authors.forename: S M
authors.initials: SM
authors.lastname: Schwartz
authors.forename: J R
authors.initials: JR
authors.lastname: Daling
authors.forename: D R
authors.initials: DR
authors.lastname: Doody
authors.forename: G C
authors.initials: GC
authors.lastname: Wipf
authors.forename: J J
authors.initials: JJ
authors.lastname: Carter
authors.forename: M M
authors.initials: MM
authors.lastname: Madeleine
authors.forename: E J
authors.initials: EJ
authors.lastname: Mao
authors.forename: E D
authors.initials: ED
authors.lastname: Fitzgibbons
authors.forename: S
authors.initials: S
authors.lastname: Huang
authors.forename: A M
authors.initials: AM
authors.lastname: Beckmann
authors.forename: J K
authors.initials: JK
authors.lastname: McDougall
authors.forename: D A
authors.initials: DA
authors.lastname: Galloway
mesh_terms: D000328:Adult; D000428:Alcohol Drinking / Q000009:adverse effects; D002294:Carcinoma, Squamous Cell / Q000821:virology*; D016022:Case-Control Studies; D004273:DNA, Neoplasm / Q000032:analysis; D004279:DNA, Viral / Q000032:analysis; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000821:virology*; D027383:Papillomaviridae / Q000235:genetics; D030361:Papillomavirus Infections / Q000150:complications* / Q000821:virology; D015995:Prevalence; D012306:Risk; D012307:Risk Factors; D012725:Sexual Behavior; D012907:Smoking / Q000009:adverse effects; D014412:Tumor Virus Infections / Q000150:complications* / Q000821:virology; D014861:Washington
chemical_list: D004273:DNA, Neoplasm; D004279:DNA, Viral