Case–Control Study of Human Papillomavirus and Oropharyngeal Cancer
This study offers persuasive evidence of a strong association between exposure to or oral infection with the human papillomavirus and oropharyngeal cancer. The data indicate that sexual behaviors can spread the virus to the oral cavity. The use of tobacco, alcohol, or both did not strengthen the ass...
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| Published in | The New England journal of medicine Vol. 356; no. 19; pp. 1944 - 1956 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Boston, MA
Massachusetts Medical Society
10.05.2007
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-4793 1533-4406 1533-4406 |
| DOI | 10.1056/NEJMoa065497 |
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| Abstract | This study offers persuasive evidence of a strong association between exposure to or oral infection with the human papillomavirus and oropharyngeal cancer. The data indicate that sexual behaviors can spread the virus to the oral cavity. The use of tobacco, alcohol, or both did not strengthen the association between exposure to HPV and oropharyngeal cancer. Among patients who had no evidence of exposure to HPV, however, tobacco and alcohol use were strongly associated with oropharyngeal cancer.
This study offers persuasive evidence of a strong association between exposure to or oral infection with HPV and oropharyngeal cancer. The use of tobacco, alcohol, or both did not strengthen the association between exposure to HPV and oropharyngeal cancer.
Infection with sexually transmitted human papillomavirus (HPV) is a cause of virtually all cervical cancers.
1
Molecular evidence also provides support for a role for HPV, particularly HPV-16, in the pathogenesis of a subgroup of squamous-cell carcinomas of the head and neck.
2
Genomic DNA of oncogenic HPV is detected in approximately 26% of all squamous-cell carcinomas of the head and neck worldwide,
3
but the molecular evidence is most rigorous and consistent for oropharyngeal squamous-cell carcinoma, in which viral integration and the expression of viral oncogenes (E6 and E7) have been shown.
4
The epidemiologic evidence of a causal role for HPV in . . . |
|---|---|
| AbstractList | Background Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent. Methods We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons. Results A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16. Conclusions Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use. [PUBLICATION ABSTRACT] Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent.BACKGROUNDSubstantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent.We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons.METHODSWe performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons.A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16.RESULTSA high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16.Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use.CONCLUSIONSOral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use. Background Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent. Methods We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons. Results A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16. Conclusions Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use. This study offers persuasive evidence of a strong association between exposure to or oral infection with the human papillomavirus and oropharyngeal cancer. The data indicate that sexual behaviors can spread the virus to the oral cavity. The use of tobacco, alcohol, or both did not strengthen the association between exposure to HPV and oropharyngeal cancer. Among patients who had no evidence of exposure to HPV, however, tobacco and alcohol use were strongly associated with oropharyngeal cancer. This study offers persuasive evidence of a strong association between exposure to or oral infection with HPV and oropharyngeal cancer. The use of tobacco, alcohol, or both did not strengthen the association between exposure to HPV and oropharyngeal cancer. Infection with sexually transmitted human papillomavirus (HPV) is a cause of virtually all cervical cancers. 1 Molecular evidence also provides support for a role for HPV, particularly HPV-16, in the pathogenesis of a subgroup of squamous-cell carcinomas of the head and neck. 2 Genomic DNA of oncogenic HPV is detected in approximately 26% of all squamous-cell carcinomas of the head and neck worldwide, 3 but the molecular evidence is most rigorous and consistent for oropharyngeal squamous-cell carcinoma, in which viral integration and the expression of viral oncogenes (E6 and E7) have been shown. 4 The epidemiologic evidence of a causal role for HPV in . . . Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent. We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons. A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16. Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use. |
| Author | Pawlita, Michael Westra, William H Viscidi, Raphael D'Souza, Gypsyamber Gillison, Maura L Fakhry, Carole Koch, Wayne M Kreimer, Aimee R |
| Author_xml | – sequence: 1 givenname: Gypsyamber surname: D'Souza fullname: D'Souza, Gypsyamber – sequence: 2 givenname: Aimee R surname: Kreimer fullname: Kreimer, Aimee R – sequence: 3 givenname: Raphael surname: Viscidi fullname: Viscidi, Raphael – sequence: 4 givenname: Michael surname: Pawlita fullname: Pawlita, Michael – sequence: 5 givenname: Carole surname: Fakhry fullname: Fakhry, Carole – sequence: 6 givenname: Wayne M surname: Koch fullname: Koch, Wayne M – sequence: 7 givenname: William H surname: Westra fullname: Westra, William H – sequence: 8 givenname: Maura L surname: Gillison fullname: Gillison, Maura L |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18737718$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17494927$$D View this record in MEDLINE/PubMed |
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| Keywords | Oropharynx cancer Papovaviridae Malignant tumor Case control study Epidemiology Infection Papillomavirus Virus Medicine Human papillomavirus Viral disease ENT disease Pharynx disease Public health |
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| Snippet | This study offers persuasive evidence of a strong association between exposure to or oral infection with the human papillomavirus and oropharyngeal cancer. The... Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic... Background Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but... |
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| SubjectTerms | Aged Alcohol Drinking - adverse effects Alcohol Drinking - epidemiology Alphapapillomavirus - isolation & purification Antibodies, Viral - blood Behavior Biological and medical sciences Cancer Carcinoma, Squamous Cell - etiology Carcinoma, Squamous Cell - pathology Carcinoma, Squamous Cell - virology Case-Control Studies Deoxyribonucleic acid DNA DNA, Viral - isolation & purification Epidemiology Family medical history Female General aspects Human papillomavirus Human papillomavirus 16 - genetics Human papillomavirus 16 - immunology Human papillomavirus 16 - isolation & purification Humans In Situ Hybridization Infections Logistic Models Male Medical sciences Middle Aged Mouth - virology Multivariate Analysis Oral Hygiene Oropharyngeal Neoplasms - etiology Oropharyngeal Neoplasms - pathology Oropharyngeal Neoplasms - virology Papillomavirus Infections - complications Public health. Hygiene Public health. Hygiene-occupational medicine Risk Factors Sexual Behavior Smoking - adverse effects Smoking - epidemiology |
| Title | Case–Control Study of Human Papillomavirus and Oropharyngeal Cancer |
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