Dataset Information

Change in Age at Diagnosis of Oropharyngeal Cancer in the United States, 1975-2016.

ABSTRACT: The emergence of the human papillomavirus (HPV) as the primary etiology of oropharyngeal cancer has changed head and neck cancer (HNC) epidemiology. This study described change in the age at diagnosis of oropharyngeal and non-oropharyngeal HNC in the United States in the last four decades. Using a retrospective cohort analysis, the Surveillance, Epidemiology, and End Results dataset from 1975 to 2016 was queried for eligible adult cases of HNC, grouped as oropharyngeal (n = 31,702) versus non-oropharyngeal (n = 87,108). Age at diagnosis was compared by gender (female, male) using independent t-test, and by race/ethnicity (Hispanic, non-Hispanic black, non-Hispanic white, non-Hispanic other) using analysis of variance. Joinpoint regression estimated yearly increases/decreases in age of diagnosis by sex and race/ethnicity through annual percent changes (APC), which were summarized with average annual percent changes (AAPC). Mean age at diagnosis for oropharyngeal cancer was 60.3 years. While there was initially a decrease in age at diagnosis, a 0.37% annual increase occurred from 2002 to 2016 (APC = 0.37, 95% confidence interval (CI) 0.28, 0.45). For non-oropharyngeal cancer, mean age at diagnosis was 63.2 years, with a continuous increase in age at diagnosis throughout the study period (1975-2016 AAPC = 0.08, 95% CI 0.04, 0.12). Females had higher average age at diagnosis than males for both sites, while blacks (57.4 years for oropharyngeal cancer; 59.0 years for non-oropharyngeal) had the lowest age at diagnosis of all races/ethnicity. Age at diagnosis of oropharyngeal cancer has increased significantly since 2002, while non-oropharyngeal HNC has increased significantly in the last four decades.

SUBMITTER: Cline BJ

PROVIDER: S-EPMC7693134 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Change in Age at Diagnosis of Oropharyngeal Cancer in the United States, 1975-2016.

Cline Brittany J BJ Simpson Matthew C MC Gropler Matthew M Bukatko Aleksandr R AR Adjei Boakye Eric E Mohammed Kahee A KA Osazuwa-Peters Nosayaba N

Cancers 20201030 11

The emergence of the human papillomavirus (HPV) as the primary etiology of oropharyngeal cancer has changed head and neck cancer (HNC) epidemiology. This study described change in the age at diagnosis of oropharyngeal and non-oropharyngeal HNC in the United States in the last four decades. Using a retrospective cohort analysis, the Surveillance, Epidemiology, and End Results dataset from 1975 to 2016 was queried for eligible adult cases of HNC, grouped as oropharyngeal (<i>n</i> = 31,702) versus ...[more]

PMID: 33143031

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Project description:ImportanceSuicide is a leading cause of death among youth aged 10 to 19 years in the United States, with rates traditionally higher in male than in female youth. Recent national mortality data suggest this gap may be narrowing, which warrants investigation.ObjectiveTo investigate trends in suicide rates among US youth aged 10 to 19 years by age group, sex, race/ethnicity, and method of suicide.Design, setting, and participantsCross-sectional study using period trend analysis of US suicide decedents aged 10 to 19 years from January 1, 1975, to December 31, 2016. Data were analyzed for periods defined by statistically significant changes in suicide rate trends. Suicide rates were calculated using population estimates.Main outcomes and measuresPeriod trends in suicide rates by sex and age group were assessed using joinpoint regression. Incidence rate ratios (IRRs) were estimated using negative binomial regression comparing male and female suicide rates within periods.ResultsFrom 1975 to 2016, we identified 85 051 youth suicide deaths in the United States (68 085 male [80.1%] and 16 966 female [19.9%]) with a male to female IRR of 3.82 (95% CI, 3.35-4.35). Following a downward trend until 2007, suicide rates for female youth showed the largest significant percentage increase compared with male youth (12.7% vs 7.1% for individuals aged 10-14 years; 7.9% vs 3.5% for individuals aged 15-19 years). The male to female IRR decreased significantly across the study period for youth aged 10 to 14 years (3.14 [95% CI, 2.74-3.61] to 1.80 [95% CI, 1.53-2.12]) and 15 to 19 years (4.15 [95% CI, 3.79-4.54] to 3.31 [95% CI, 2.96-3.69]). Significant declining trends in the male to female IRR were found in non-Hispanic white youth aged 10 to 14 years (3.27 [95% CI, 2.68-4.00] to 2.04 [95% CI, 1.45-2.89]) and non-Hispanic youth of other races aged 15 to 19 years (4.02 [95% CI, 3.29-4.92] to 2.35 [95% CI, 2.00-2.76]). The male to female IRR for firearms increased significantly for youth aged 15 to 19 years (χ2 = 7.74; P = .02 for sex × period interaction). The male to female IRR of suicide by hanging or suffocation decreased significantly for both age groups (10-14 years: χ2 = 88.83; P < .001 for sex × period interaction and 15-19 years: χ2 = 82.15; P < .001 for sex × period interaction). No significant change was found in the male to female IRR of suicide by poisoning across the study period.Conclusions and relevanceA significant reduction in the historically large gap in youth suicide rates between male and female individuals underscores the importance of interventions that consider unique differences by sex. Future research examining sex-specific factors associated with youth suicide is warranted.

Project description:BackgroundStudies have reported young ages at cancer diagnosis in HIV-infected persons and have suggested that HIV accelerates carcinogenesis. However, these comparisons did not account for differences in population age structures.ObjectiveTo compare ages at diagnosis for non-AIDS-defining types of cancer that occur in both the AIDS and general populations, after adjustment for differences in age and other demographic characteristics between these populations.DesignRegistry linkage study.Setting15 HIV/AIDS and cancer registry databases in the United States.Participants212 055 persons with AIDS enrolled in the U.S. HIV/AIDS Cancer Match Study from 1996 to 2007.MeasurementsComparison of age-at-diagnosis distributions for various types of cancer in both the AIDS and general populations, after adjustment for age and other demographic characteristics.ResultsThe proportion of person-time contributed by older persons (age ≥65 years) was far smaller in the AIDS population (1.5%) than in the general population (12.5%). Reflecting this difference, the ages at diagnosis for most types of cancer were approximately 20 years younger among persons with AIDS. However, after adjustment for differences in the populations at risk, the median ages at diagnosis in the AIDS and general populations did not differ for most types of cancer (for example, colon, prostate, or breast cancer; all P > 0.100). In contrast, ages at diagnosis of lung (median, 50 vs. 54 years) and anal cancer (median, 42 vs. 45 years) were significantly younger in persons with AIDS than expected in the general population (P < 0.001), and the age at diagnosis of Hodgkin lymphoma was significantly older (median, 42 vs. 40 years; P < 0.001).LimitationsInformation on other cancer risk factors, including cigarette smoking, was not available. Analysis was restricted to non-Hispanic white and black persons who had AIDS, which could limit the generalizability of the findings to other racial and ethnic groups or to persons with HIV but not AIDS.ConclusionFor most types of cancer, the age at diagnosis is similar in the AIDS and general populations, after adjustment for the ages of the populations at risk. Modest age differences remained for a few types of cancer, which may indicate either acceleration of carcinogenesis by HIV or earlier exposure to cancer risk factors.Primary funding sourceNational Cancer Institute.

Project description:PurposeRecent 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 methodsHPV 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.ResultsHPV 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.ConclusionIncreases in the population-level incidence and survival of oropharyngeal cancers in the United States since 1984 are caused by HPV infection.

Dataset Information

Change in Age at Diagnosis of Oropharyngeal Cancer in the United States, 1975-2016.

Publications

Change in Age at Diagnosis of Oropharyngeal Cancer in the United States, 1975-2016.

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