Distinct Risk Factor Profiles for Human Papillomavirus Type 16–Positive and Human Papillomavirus Type 16–Negative Head and Neck Cancers
Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16–positive HNSCCs are similar to those for HPV-16–negative HNSCCs in a hospital-based case–control study. Met...
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| Published in | JNCI : Journal of the National Cancer Institute Vol. 100; no. 6; pp. 407 - 420 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cary, NC
Oxford University Press
19.03.2008
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8874 1460-2105 1460-2105 |
| DOI | 10.1093/jnci/djn025 |
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| Abstract | Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16–positive HNSCCs are similar to those for HPV-16–negative HNSCCs in a hospital-based case–control study. Methods Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16–positive and HPV-16–negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16–positive HNSCC and HPV-16–negative HNSCC associated with risk factors. All statistical tests were two-sided. Results HPV-16 was detected in 92 of 240 case subjects. HPV-16–positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (Ptrend = .01) and with increasing intensity (joints per month, Ptrend = .007), duration (in years, Ptrend = .01), and cumulative joint-years (Ptrend = .003) of marijuana use. By contrast, HPV-16–negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, Ptrend < .001), increasing years of heavy alcohol drinking (≥15 years of 14 drinks per week; Ptrend = .03), and increasing number of lost teeth (Ptrend = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (≥20 pack-years) and alcohol had an increased risk of HPV-16–negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16–positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). Conclusions HPV-16–positive HNSCCs and HPV-16–negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. |
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| AbstractList | Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16–positive HNSCCs are similar to those for HPV-16–negative HNSCCs in a hospital-based case–control study. Methods Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16–positive and HPV-16–negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16–positive HNSCC and HPV-16–negative HNSCC associated with risk factors. All statistical tests were two-sided. Results HPV-16 was detected in 92 of 240 case subjects. HPV-16–positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (Ptrend = .01) and with increasing intensity (joints per month, Ptrend = .007), duration (in years, Ptrend = .01), and cumulative joint-years (Ptrend = .003) of marijuana use. By contrast, HPV-16–negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, Ptrend < .001), increasing years of heavy alcohol drinking (≥15 years of 14 drinks per week; Ptrend = .03), and increasing number of lost teeth (Ptrend = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (≥20 pack-years) and alcohol had an increased risk of HPV-16–negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16–positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). Conclusions HPV-16–positive HNSCCs and HPV-16–negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study.BACKGROUNDHigh-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study.Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided.METHODSCase subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided.HPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (P(trend) = .01) and with increasing intensity (joints per month, P(trend) = .007), duration (in years, P(trend) = .01), and cumulative joint-years (P(trend) = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, P(trend) < .001), increasing years of heavy alcohol drinking (> or = 15 years of 14 drinks per week; P(trend) = .03), and increasing number of lost teeth (P(trend) = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (> or = 20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9).RESULTSHPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (P(trend) = .01) and with increasing intensity (joints per month, P(trend) = .007), duration (in years, P(trend) = .01), and cumulative joint-years (P(trend) = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, P(trend) < .001), increasing years of heavy alcohol drinking (> or = 15 years of 14 drinks per week; P(trend) = .03), and increasing number of lost teeth (P(trend) = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (> or = 20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9).HPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers.CONCLUSIONSHPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. Background: High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study. Methods: Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided. Results: HPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (Ptrend = .01) and with increasing intensity (joints per month, Ptrend = .007), duration (in years, Ptrend = .01), and cumulative joint-years (Ptrend = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, Ptrend < .001), increasing years of heavy alcohol drinking (≥15 years of 14 drinks per week; Ptrend = .03), and increasing number of lost teeth (Ptrend = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (≥20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). Conclusions: HPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. [PUBLICATION ABSTRACT] High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study. Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided. HPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (P(trend) = .01) and with increasing intensity (joints per month, P(trend) = .007), duration (in years, P(trend) = .01), and cumulative joint-years (P(trend) = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, P(trend) < .001), increasing years of heavy alcohol drinking (> or = 15 years of 14 drinks per week; P(trend) = .03), and increasing number of lost teeth (P(trend) = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (> or = 20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). HPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study. Methods Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided. Results HPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (P trend = .01) and with increasing intensity (joints per month, P trend = .007), duration (in years, P trend = .01), and cumulative joint-years (P trend = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, P trend < .001), increasing years of heavy alcohol drinking (≥15 years of 14 drinks per week; P trend = .03), and increasing number of lost teeth (P trend = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco (≥20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). Conclusions HPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. BACKGROUND: High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the risk factors for HPV-16-positive HNSCCs are similar to those for HPV-16-negative HNSCCs in a hospital-based case-control study. METHODS: Case subjects (n = 240) diagnosed with HNSCC at the Johns Hopkins Hospital from 2000 through 2006 were stratified by tumor HPV-16 status as determined by in situ hybridization. Two control subjects (n = 322) without cancer were individually matched by age and sex to each HPV-16-positive and HPV-16-negative case subject. Data on risk behaviors were obtained by use of audio computer-assisted self-interview technology. Multivariable conditional logistic regression models were used to estimate the odds ratios (ORs) for HPV-16-positive HNSCC and HPV-16-negative HNSCC associated with risk factors. All statistical tests were two-sided. RESULTS: HPV-16 was detected in 92 of 240 case subjects. HPV-16-positive HNSCC was independently associated with several measures of sexual behavior and exposure to marijuana but not with cumulative measures of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with increasing number of oral sex partners (P sub(trend) = .01) and with increasing intensity (joints per month, P sub(trend) = .007), duration (in years, P sub(trend) = .01), and cumulative joint-years (P sub(trend) = .003) of marijuana use. By contrast, HPV-16-negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor oral hygiene but not with any measure of sexual behavior or marijuana use. Associations increased in strength with increasing intensity (cigarettes per day), duration, and cumulative pack-years of tobacco smoking (for all, P sub(trend) < .001), increasing years of heavy alcohol drinking ( greater than or equal to 15 years of 14 drinks per week; P sub(trend) = .03), and increasing number of lost teeth (P sub(trend) = .001). Compared with subjects who neither smoked tobacco nor drank alcohol, those with heavy use of tobacco ( greater than or equal to 20 pack-years) and alcohol had an increased risk of HPV-16-negative HNSCC (OR = 4.8, 95% confidence interval [CI] = 1.8 to 12) but not of HPV-16-positive HNSCC (OR = 0.67, 95% CI = 0.29 to 1.9). CONCLUSIONS: HPV-16-positive HNSCCs and HPV-16-negative HNSCCs have different risk factor profiles, indicating that they should be considered to be distinct cancers. |
| Author | Westra, William Viscidi, Raphael D'Souza, Gypsyamber Xiao, Weihong Gillison, Maura L. Sugar, Elizabeth Begum, Shahnaz |
| Author_xml | – sequence: 1 givenname: Maura L. surname: Gillison fullname: Gillison, Maura L. email: gillima@jhmi.edu organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 2 givenname: Gypsyamber surname: D'Souza fullname: D'Souza, Gypsyamber organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 3 givenname: William surname: Westra fullname: Westra, William organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 4 givenname: Elizabeth surname: Sugar fullname: Sugar, Elizabeth organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 5 givenname: Weihong surname: Xiao fullname: Xiao, Weihong organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 6 givenname: Shahnaz surname: Begum fullname: Begum, Shahnaz organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD – sequence: 7 givenname: Raphael surname: Viscidi fullname: Viscidi, Raphael organization: Affiliations of authors: Divisions of Viral Oncology (MLG, WX) and Biometry and Oncology Biostatistics (ES), The Johns Hopkins Kimmel Comprehensive Cancer Center, Baltimore, MD; Department of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (GDS); Departments of Pathology (WW, SB) and Pediatrics (RV), Johns Hopkins Hospital, Baltimore, MD |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20368436$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/18334711$$D View this record in MEDLINE/PubMed |
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| Snippet | Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined... Background High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined... High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined whether the... Background: High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined... BACKGROUND: High-risk types of human papillomavirus (HPV), including HPV-16, cause a subgroup of head and neck squamous cell carcinomas (HNSCCs). We examined... |
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| SubjectTerms | Adult Aged Alcohol Drinking - adverse effects Alphapapillomavirus - isolation & purification Antibodies, Viral - blood Biological and medical sciences Capsid Proteins - blood Carcinoma, Squamous Cell - etiology Carcinoma, Squamous Cell - virology Case-Control Studies DNA, Viral - isolation & purification Female Head & neck cancer Head and Neck Neoplasms - etiology Head and Neck Neoplasms - virology Human papillomavirus Human papillomavirus 16 - genetics Human papillomavirus 16 - immunology Human papillomavirus 16 - isolation & purification Humans Male Marijuana Smoking - adverse effects Medical sciences Middle Aged Odds Ratio Oncology Oral Hygiene - adverse effects Otorhinolaryngology (head neck, general aspects and miscellaneous) Otorhinolaryngology. Stomatology Pathology Risk Assessment Risk Factors Sexual Behavior Smoking - adverse effects Tumors Viral Load |
| Title | Distinct Risk Factor Profiles for Human Papillomavirus Type 16–Positive and Human Papillomavirus Type 16–Negative Head and Neck Cancers |
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