scholarly journals Human Papillomavirus and Rising Oropharyngeal Cancer Incidence in the United States

2011 ◽  
Vol 29 (32) ◽  
pp. 4294-4301 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Eric A. Engels ◽  
Ruth M. Pfeiffer ◽  
Brenda Y. Hernandez ◽  
Weihong Xiao ◽  
...  

Purpose Recent increases in incidence and survival of oropharyngeal cancers in the United States have been attributed to human papillomavirus (HPV) infection, but empirical evidence is lacking. Patients and Methods HPV status was determined for all 271 oropharyngeal cancers (1984-2004) collected by the three population-based cancer registries in the Surveillance, Epidemiology, and End Results (SEER) Residual Tissue Repositories Program by using polymerase chain reaction and genotyping (Inno-LiPA), HPV16 viral load, and HPV16 mRNA expression. Trends in HPV prevalence across four calendar periods were estimated by using logistic regression. Observed HPV prevalence was reweighted to all oropharyngeal cancers within the cancer registries to account for nonrandom selection and to calculate incidence trends. Survival of HPV-positive and HPV-negative patients was compared by using Kaplan-Meier and multivariable Cox regression analyses. Results HPV prevalence in oropharyngeal cancers significantly increased over calendar time regardless of HPV detection assay (P trend < .05). For example, HPV prevalence by Inno-LiPA increased from 16.3% during 1984 to 1989 to 71.7% during 2000 to 2004. Median survival was significantly longer for HPV-positive than for HPV-negative patients (131 v 20 months; log-rank P < .001; adjusted hazard ratio, 0.31; 95% CI, 0.21 to 0.46). Survival significantly increased across calendar periods for HPV-positive (P = .003) but not for HPV-negative patients (P = .18). Population-level incidence of HPV-positive oropharyngeal cancers increased by 225% (95% CI, 208% to 242%) from 1988 to 2004 (from 0.8 per 100,000 to 2.6 per 100,000), and incidence for HPV-negative cancers declined by 50% (95% CI, 47% to 53%; from 2.0 per 100,000 to 1.0 per 100,000). If recent incidence trends continue, the annual number of HPV-positive oropharyngeal cancers is expected to surpass the annual number of cervical cancers by the year 2020. Conclusion Increases in the population-level incidence and survival of oropharyngeal cancers in the United States since 1984 are caused by HPV infection.

2019 ◽  
Vol 37 (18) ◽  
pp. 1538-1546 ◽  
Author(s):  
Joseph E. Tota ◽  
Ana F. Best ◽  
Zachary S. Zumsteg ◽  
Maura L. Gillison ◽  
Philip S. Rosenberg ◽  
...  

PURPOSE Human papillomavirus–positive oropharynx cancer incidence has increased rapidly in cohorts of US white men born during the 1930s to 1950s. It is unknown how the trajectory of the oropharynx cancer epidemic may be changing in the United States. METHODS Using US cancer registry information, we investigated whether increases in oropharynx cancer have continued into recent birth cohorts and forecasted the future burden across age, sex, and race/ethnicity subgroups. Log-linear Joinpoint regression and age-period-cohort models were used to evaluate incidence trends during 1992 to 2015 and projections through 2029. RESULTS Among white men, oropharynx cancer incidence increased rapidly in individuals born during 1939 to 1955 (5.3% per 2-year birth cohort; 95% CI, 4.8% to 5.7%), but this rate of increase significantly moderated in individuals born during 1955 to 1969 (1.7% per 2-year birth cohort; 95% CI, 1.0% to 2.4%). Should these birth-cohort trends continue, from 2016 to 2029 we forecast that incidence will increase dramatically in older white men 65 to 74 years of age (from 40.7 to 71.2 per 100,000) and 75 to 84 years of age (from 25.7 to 50.1 per 100,000), moderately in white men 55 to 64 years of age (from 40.3 to 52.0 per 100,000), and remain stable in white men 45 to 54 years of age (approximately 18 per 100,000). Accounting for population growth, we project an increase in annual number of cases in the United States from 20,124 (95% CI, 19,779 to 20,469) in 2016 to 30,629 (95% CI, 29,413 to 31,845) in 2029, primarily driven by older individuals (age ≥ 65 years; from 7,976 [95% CI, 7,782 to 8,172] to 18,072 [95% CI, 17,271 to 18,895]) and white men (from 14,453 [95% CI, 14,142 to 14,764] to 22,241 [95% CI, 21,119 to 23,364]). CONCLUSION The exponential increase in oropharynx cancer incidence in young white US men has ebbed, and modest increases are occurring/anticipated in cohorts born after 1955. Continued strong increases in incidence in cohorts born before 1955, and an approximate 50% increase in size of the US population age 65 years or older through 2029, portend a substantial shift in burden to elderly white men.


Vaccines ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 366
Author(s):  
Houssein H. Ayoub ◽  
Hiam Chemaitelly ◽  
Laith J. Abu-Raddad

This study aims to inform herpes simplex virus type 2 (HSV-2) vaccine development, licensure, and implementation by delineating the population-level impact of vaccination. Mathematical models were constructed to describe the transmission dynamics in presence of prophylactic or therapeutic vaccines assuming 50% efficacy, with application to the United States. Catch-up prophylactic vaccination will reduce, by 2050, annual number of new infections by 58%, incidence rate by 60%, seroprevalence by 21%, and avert yearly as much as 350,000 infections. Number of vaccinations needed to avert one infection was only 50 by 2050, 34 by prioritizing those aged 15–19 years, 4 by prioritizing the highest sexual risk group, 43 by prioritizing women, and 47 by prioritizing men. Therapeutic vaccination of infected adults with symptomatic disease will reduce, by 2050, annual number of new infections by 12%, incidence rate by 13%, seroprevalence by 4%, and avert yearly as much as 76,000 infections. Number of vaccinations needed to avert one infection was eight by 2050, two by prioritizing those aged 15–19 years, three by prioritizing the highest sexual risk group, seven by prioritizing men, and ten by prioritizing women. HSV-2 vaccination offers an impactful and cost-effective intervention to prevent genital herpes medical and psychosexual disease burden.


2018 ◽  
Vol 36 (3) ◽  
pp. 262-267 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Barry I. Graubard ◽  
Tatevik Broutian ◽  
Robert K.L. Pickard ◽  
Zhen-Yue Tong ◽  
...  

Purpose The incidence of human papilloma virus (HPV)–positive oropharyngeal cancers has risen rapidly in recent decades among men in the United States. We investigated the US population–level effect of prophylactic HPV vaccination on the burden of oral HPV infection, the principal cause of HPV-positive oropharyngeal cancers. Methods We conducted a cross-sectional study of men and women 18 to 33 years of age (N = 2,627) within the National Health and Nutrition Examination Survey 2011 to 2014, a representative sample of the US population. Oral HPV infection with vaccine types 16, 18, 6, or 11 was compared by HPV vaccination status, as measured by self-reported receipt of at least one dose of the HPV vaccine. Analyses accounted for the complex sampling design and were adjusted for age, sex, and race. Statistical significance was assessed using a quasi-score test. Results Between 2011 and 2014, 18.3% of the US population 18 to 33 years of age reported receipt of at least one dose of the HPV vaccine before the age of 26 years (29.2% in women and 6.9% in men; P < .001). The prevalence of oral HPV16/18/6/11 infections was significantly reduced in vaccinated versus unvaccinated individuals (0.11% v 1.61%; Padj = .008), corresponding to an estimated 88.2% (95% CI, 5.7% to 98.5%) reduction in prevalence after model adjustment for age, sex, and race. Notably, the prevalence of oral HPV16/18/6/11 infections was significantly reduced in vaccinated versus unvaccinated men (0.0% v 2.13%; Padj = .007). Accounting for vaccine uptake, the population-level effect of HPV vaccination on the burden of oral HPV16/18/6/11 infections was 17.0% overall, 25.0% in women, and 6.9% in men. Conclusion HPV vaccination was associated with reduction in vaccine-type oral HPV prevalence among young US adults. However, because of low vaccine uptake, the population-level effect was modest overall and particularly low in men.


2008 ◽  
Vol 26 (4) ◽  
pp. 612-619 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Eric A. Engels ◽  
William F. Anderson ◽  
Maura L. Gillison

Purpose To investigate the impact of human papillomavirus (HPV) on the epidemiology of oral squamous cell carcinomas (OSCCs) in the United States, we assessed differences in patient characteristics, incidence, and survival between potentially HPV-related and HPV-unrelated OSCC sites. Patients and Methods Data from nine Surveillance, Epidemiology, and End Results program registries (1973 to 2004) were used to classify OSCCs by anatomic site as potentially HPV-related (n = 17,625) or HPV-unrelated (n = 28,144). Joinpoint regression and age-period-cohort models were used to assess incidence trends. Life-table analyses were used to compare 2-year overall survival for HPV-related and HPV-unrelated OSCCs. Results HPV-related OSCCs were diagnosed at younger ages than HPV-unrelated OSCCs (mean ages at diagnosis, 61.0 and 63.8 years, respectively; P < .001). Incidence increased significantly for HPV-related OSCC from 1973 to 2004 (annual percentage change [APC] = 0.80; P < .001), particularly among white men and at younger ages. By contrast, incidence for HPV-unrelated OSCC was stable through 1982 (APC = 0.82; P = .186) and declined significantly during 1983 to 2004 (APC = −1.85; P < .001). When treated with radiation, improvements in 2-year survival across calendar periods were more pronounced for HPV-related OSCCs (absolute increase in survival from 1973 through 1982 to 1993 through 2004 for localized, regional, and distant stages = 9.9%, 23.1%, and 18.6%, respectively) than HPV-unrelated OSCCs (5.6%, 3.1%, and 9.9%, respectively). During 1993 to 2004, for all stages treated with radiation, patients with HPV-related OSCCs had significantly higher survival rates than those with HPV-unrelated OSCCs. Conclusion The proportion of OSCCs that are potentially HPV-related increased in the United States from 1973 to 2004, perhaps as a result of changing sexual behaviors. Recent improvements in survival with radiotherapy may be due in part to a shift in the etiology of OSCCs.


2020 ◽  
Vol 146 (11) ◽  
pp. 3026-3033 ◽  
Author(s):  
Deepti Bettampadi ◽  
Luisa L. Villa ◽  
Eduardo L. Ponce ◽  
Jorge Salmeron ◽  
Bradley A. Sirak ◽  
...  

Author(s):  
James Custer ◽  
Riddhi Patel ◽  
George L Delclos ◽  
Stacia M DeSantis

Abstract Background Oropharyngeal cancers associated with high-risk human papillomavirus (HR-HPV) infection are increasing in the United States, especially among men. We evaluated the prevalence and predictors of concurrent (genital and oral) and concordant (same-type) HR-HPV infections in the United States. Methods We used the National Health and Nutrition Examination Survey from 2009 to 2016. Predictors were assessed via multivariable logistic regression. Results Among 10 334 respondents, 172 (2.1%) had concurrent infections (109 [3.5%] men and 63 [0.76%] women]. Ninety-three (1.0%) had concordant infections (54 [1.6%] men and 39 [0.5%] women). Predictors of concurrence in men included the following: no longer married versus married (odds ratio [OR], 2.3; 95% confidence interval [CI], 1.3–4.9), living with a partner versus married (3.0; 1.2–7.5), and having 2–5 lifetime oral sex partners (3.0; 1.2–7.5). In women they included the following: no longer married versus married (3.6; 1.3–10.3), ≥2 recent sex partners (4.6; 1.4–15.6 for 2–5 partners and 3.9; 1.1–14.3 for ≥6 partners), and marijuana use (2.2; 1.0–4.5). The predictor of concordance in men and women was no longer married versus married (3.5; 1.2–9.9 in men and 3.2; 1.1–9.4 in women). Conclusions Concurrent and concordant HR-HPV infections occur at a high rate, especially among men, and are associated with behavioral factors. This underscores the importance of HPV vaccination, screening, and education in men.


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