The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Oral Cancer Risk in Relation to Sexual History and Evidence of Human Papillomavirus Infection
Open accessAbstract
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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Cites
Primer-Directed Enzymatic Amplification of DNA with a Thermostable DNA Polymerase
Saiki, R. K., Gelfand, D. H., Stoffel, S., Scharf, S. J., Higuchi, R., Horn, G. T., Mullis, K. B., & Erlich, H. A. (1988) · Science · doi:10.1126/science.2448875 · Cited by 17,719
Confidence interval estimation of interaction
Hosmer, D. W., & Lemeshow, S. (1992) · Epidemiology · doi:10.1097/00001648-199209000-00012 · Cited by 1,239
Statistical Analysis of Case-Control Studies
Thompson, W. D. (1994) · Epidemiologic Reviews · doi:10.1093/oxfordjournals.epirev.a036143 · Cited by 117
Cited by
Gillison, M. L., D'Souza, G., Westra, W., Sugar, E., Xiao, W., Begum, S., & Viscidi, R. (2008) · JNCI: Journal of the National Cancer Institute · doi:10.1093/jnci/djn025 · Cited by 1,543
Papillomaviruses in the causation of human cancers - a brief historical account
zur Hausen, H. (2009) · Virology · doi:10.1016/j.virol.2008.11.046 · Cited by 1,532
Human Papillomavirus Infection as a Risk Factor for Squamous-Cell Carcinoma of the Head and Neck
Mork, J., Lie, A. K., Glattre, E., Clark, S., Hallmans, G., Jellum, E., Koskela, P., Møller, B., Pukkala, E., Schiller, J. T., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200104123441503 · Cited by 939
Ndiaye, C., Mena, M., Alemany, L., Arbyn, M., Castellsagué, X., Laporte, L., Bosch, F. X., de Sanjosé, S., & Trottier, H. (2014) · The Lancet Oncology · doi:10.1016/s1470-2045(14)70471-1 · Cited by 722
Rampias, T., Sasaki, C., Weinberger, P., & Psyrri, A. (2009) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djp017 · Cited by 264
Metadata
- Authors
- Schwartz, S. M., Daling, J. R., Madeleine, M. M., Doody, D. R., Fitzgibbons, E. D., Wipf, G. C., Carter, J. J., Mao, E.-J., Huang, S., Beckmann, A. M., McDougall, J. K., & Galloway, D. A.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 1998-11-04
- Volume
- 90
- Issue
- 21
- Pages
- 1626-1636
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2170019502
- Cited by
- 588
- References
- 3
- FWCI
- 15.71
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Schwartz, S. M., Daling, J. R., Madeleine, M. M., Doody, D. R., Fitzgibbons, E. D., Wipf, G. C., Carter, J. J., Mao, E.-J., Huang, S., Beckmann, A. M., McDougall, J. K., & Galloway, D. A. (1998). Oral Cancer Risk in Relation to Sexual History and Evidence of Human Papillomavirus Infection. JNCI Journal of the National Cancer Institute. https://doi.org/10.1093/jnci/90.21.1626
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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