This study sought to determine the prevaccine type-specific prevalence of human papillomavirus (HPV)–associated cancers in the United States to evaluate the potential impact of the HPV types in the current and newly approved 9-valent HPV vaccines. The Centers for Disease Control and Prevention partnered with seven US population-based cancer registries to obtain archival tissue for cancers diagnosed from 1993 to 2005. HPV testing was performed on 2670 case patients that were fairly representative of all participating cancer registry cases by age and sex. Demographic and clinical data were evaluated by anatomic site and HPV status. Current US cancer registry data and the detection of HPV types were used to estimate the number of cancers potentially preventable through vaccination. HPV DNA was detected in 90.6% of cervical, 91.1% of anal, 75.0% of vaginal, 70.1% of oropharyngeal, 68.8% of vulvar, 63.3% of penile, 32.0% of oral cavity, and 20.9% of laryngeal cancers, as well as in 98.8% of cervical cancer in situ (CCIS). A vaccine targeting HPV 16/18 potentially prevents the majority of invasive cervical (66.2%), anal (79.4%), oropharyngeal (60.2%), and vaginal (55.1%) cancers, as well as many penile (47.9%), vulvar (48.6%) cancers: 24 858 cases annually. The 9-valent vaccine also targeting HPV 31/33/45/52/58 may prevent an additional 4.2% to 18.3% of cancers: 3944 cases annually. For most cancers, younger age at diagnosis was associated with higher HPV 16/18 prevalence. With the exception of oropharyngeal cancers and CCIS, HPV 16/18 prevalence was similar across racial/ethnic groups. In the United States, current vaccines will reduce most HPV-associated cancers; a smaller additional reduction would be contributed by the new 9-valent vaccine.

BACKGROUND. As human papillomavirus (HPV) vaccination becomes widely available in the US for cervical cancer prevention, it may also affect the rates of other cancers potentially associated with HPV. The objective of the current study was to describe the incidence rates of oropharyngeal and oral cavity cancers in the US with a focus on anatomic sites potentially associated with HPV infection. METHODS. Incident cases diagnosed between 1998 and 2003 identified through 39 population-based registries that participate in the National Program of Cancer Registries and/or the Surveillance, Epidemiology, and End Results Program were examined. The incidence rates of potentially HPV-associated oropharyngeal and oral cavity cancers by various characteristics were estimated. The 1998 through 2003 trends in these rates were also compared with rates for sites not previously shown to be associated with HPV (comparison sites). RESULTS. In all, 44,160 cases of potentially HPV-associated cancers of the oropharynx and oral cavity were identified, including 19,239 (43.6%) tonsillar, 16,964 (38.4%) base of tongue, and 7957 (18.0%) other oropharyngeal cancers. The incidence rates for these sites were highest among blacks, and higher among non-Hispanics and men than among Hispanics and women. The annual incidence rates of potentially HPV-associated cancers of the tonsil and base of tongue both increased significantly from 1998 through 2003 (annual percentage change [APC], 3.0; P < .05 for both sites), whereas the incidence rates of cancer at the comparison sites generally decreased. CONCLUSIONS. The results of the current study provide baseline incidence rates of potentially HPV-associated cancers of the oropharynx and oral cavity that can be compared with rates after the widespread implementation of the HPV vaccination. Cancer 2008;113(10 suppl):2901–9. Published 2008 by the American Cancer Society.

Human papillomavirus type 16 (HPV16) seropositivity and alcohol and tobacco use have been associated with risk of head and neck squamous cell carcinoma (HNSCC). However, it is less clear whether HPV16 influences HNSCC risk associated with alcohol and tobacco use. Incident cases of HNSCC diagnosed between December 1999 and December 2003 were identified from nine medical facilities in Greater Boston, MA. Control subjects were frequency matched to case subjects on age, sex, and town of residence. A total of 485 case subjects and 549 control subjects reported information on lifetime smoking and alcohol consumption and provided sera, which was used to determine presence of HPV16 antibodies. Unconditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) of HNSCC risk by alcohol consumption (drinks per week: <3, 3 to <8, 8 to 0 to <20, 20 to <45, ≥45), adjusting for age, sex, race, education, and HPV16 serology. Polytomous logistic regression was used to estimate odds ratios and 95% confidence intervals for the association of HPV16 serology, alcohol consumption, and tobacco use in site-specific analyses. All statistical tests were two-sided. The strongest risk factors by tumor site were smoking for laryngeal cancer, alcohol for cancer of the oral cavity, and HPV16 for pharyngeal cancer. For pharyngeal cancer, risk increased with increasing alcohol consumption (OR_{≥25 versus <3 drinks per week} = 5.1, 95% CI = 2.4 to 11.0) and smoking (OR_{≥45 pack-years versus never smoker} = 6.9, 95% CI = 3.1 to 15.1) among HPV16-seronegative subjects but not among HPV16-seropositive subjects (P_{interaction, HPV16 serology and alcohol} = .002; P_{interaction, HPV16 serology and smoking} = .007). Among light drinkers or never smokers, HPV16 seropositivity was associated with a 30-fold increased risk of pharyngeal cancer. Alcohol or tobacco use does not further increase risk of HPV16-associated pharyngeal cancer. HNSCC risk associated with smoking, alcohol, and HPV16 differs by tumor site.

Promoter methylation is an important pathway in transcriptional silencing of known and candidate tumor suppressor genes in Head and Neck Squamous Cell Carcinoma (HNSCC). In order to study the association of tumor suppressor gene promoter methylation in HNSCC with patient clinical characteristics, especially alcohol consumption and tobacco smoking, we examined promoter methylation of the p16^INK4a, DAP-kinase, E-Cadherin, and RASSF1A genes using methylation-specific PCR (MSP) in 80 patients. The prevalence of p16^INK4a, DAP-kinase, E-Cadherin, and RASSF1A promoter methylation was 26/80 (32.5%), 19/80 (23.8%), 29/80 (36.3%), 6/80 (7.5%) respectively. In 48 cases (60%), at least one of these promoters was methylated. There was a significant association of methylation of any of these genes and ever smoking (P=0.006). p16^INK4a gene promoter methylation was associated with a younger age of smoking initiation (P<0.03); E-Cadherin promoter methylation was associated with an increased number of pack years smoked (P<0.03). We also found an association of methylation of any gene and T status (OR=2.7, P<0.05). Tumors with p16^INK4a methylation were significantly less likely to show lymph node metastasis (P<0.001). DAP-kinase promoter methylation was significantly associated with lymph node metastasis and this relationship was dependent upon p16^INK4a promoter methylation status. Our results suggest that, in HNSCC, promoter methylation of these four genes accumulates with increasing tumor size. This may reflect distinct pathways of somatic inactivation leading to cancer; additional larger studies are needed to further investigate this possibility. Tobacco smoking may play an important role in both the occurrence of promoter methylation as well as delineating the precise pathway that eventually results in a tumorigenic phenotype.

Background: Louisiana in the summer of 2020 had the highest per capita case count for COVID-19 in the United States and COVID-19 deaths disproportionately affects the African American population. Neighborhood deprivation has been observed to be associated with poorer health outcomes. The purpose of this study was to examine the relationship between neighborhood deprivation and COVID-19 in Louisiana. Methods: The Area Deprivation Index (ADI) was calculated and used to classify neighborhood deprivation at the census tract level. A total of 17 US census variables were used to calculate the ADI for each of the 1148 census tracts in Louisiana. The data were extracted from the American Community Survey (ACS) 2018. The neighborhoods were categorized into quintiles as well as low and high deprivation. The publicly available COVID-19 cumulative case counts by census tract were obtained from the Louisiana Department of Health website on July 31, 2020. Descriptive and Poisson regression analyses were performed. Results: Neighborhoods in Louisiana were substantially different with respect to deprivation. The ADI ranged from 136.00 for the most deprived neighborhood and –33.87 in the least deprived neighborhood. We observed that individuals residing in the most deprived neighborhoods had almost a 40% higher risk of COVID-19 compared to those residing in the least deprived neighborhoods. Conclusion: While the majority of previous studies were focused on very limited socio-environmental factors such as crowding and income, this study used a composite area-based deprivation index to examine the role of neighborhood environment on COVID-19. We observed a positive relationship between neighborhood deprivation and COVID-19 risk in Louisiana. The study findings can be utilized to promote public health preventions measures besides social distancing, wearing a mask while in public and frequent handwashing in vulnerable neighborhoods with greater deprivation.

Evidence suggests that human papillomavirus (HPV)16 seropositivity reflects past HPV16 exposure and is associated with risk for head and neck squamous cell carcinoma (HNSCC). Our objectives were to test the hypothesis that HPV16 seropositivity is associated with risk for HNSCC, to correlate HPV16 seropositivity with HPV16 tumor DNA, and to correlate HPV16 seropositivity and HPV16 DNA with sexual history and patient survival. In a case–control study of approximately 1,000 individuals, we assessed serology to the HPV16 L1 protein and in cases only, assayed tumors for HPV16 DNA. HPV16 seropositivity was associated with 1.5‐ and 6‐fold risks for tumors of the oral cavity and pharynx, respectively. There was a dose response trend for HPV16 titer and increasing risk of HNSCC (p < 0.0001) and HPV16 tumor DNA (p < 0.0001). In cases, HPV16 DNA and seropositivity were significantly associated with sexual activity; odds ratios (ORs) of 12.8 and 3.7 were observed for more than 10 oral sexual partners and ORs of 4.5 and 3.2 were associated with a high number of lifetime sexual partners, respectively. Finally, HPV16 seropositivity and HPV16 tumor DNA were associated with hazard ratios of 0.4 and 0.5, respectively, indicating better survival for HPV positive individuals. HPV16 seropositivity was associated with risk for HNSCC, with greatest risk for pharyngeal cancer. We observed dose response relationships between serology titer and both risk for HNSCC and HPV16 tumor DNA. In cases, HPV16 tumor DNA and positive serology were associated with sexual history and improved disease free survival.