Mona Saraiya1, Elizabeth R Unger2, Trevor D Thompson2, Charles F Lynch2, Brenda Y Hernandez2, Christopher W Lyu2, Martin Steinau2, Meg Watson2, Edward J Wilkinson2, Claudia Hopenhayn2, Glenn Copeland2, Wendy Cozen2, Edward S Peters2, Youjie Huang2, Maria Sibug Saber2, Sean Altekruse2, Marc T Goodman2. 1. Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion (MSa, TDT, MW) and Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases (ERU, MSt), Centers for Disease Control and Prevention, Atlanta, GA; University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI (MTG, BYH); Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, IA (CFL); Departments of Preventive Medicine (WC) and Pathology (WC, MSS), University of Southern California, Los Angeles, CA; Department of Epidemiology, School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA (ESP); Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL (EJW); Michigan Department of Community Health, Lansing, MI (GC); Department of Epidemiology, College of Public Health, University of Kentucky, Lexington, KY (CH); Florida Department of Health, Tallahassee, FL (YH); Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD (SFA); Battelle Memorial Institute, Durham, NC (CWL); National Cancer Institute (SA). msaraiya@cdc.gov. 2. Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion (MSa, TDT, MW) and Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases (ERU, MSt), Centers for Disease Control and Prevention, Atlanta, GA; University of Hawaii Cancer Center, University of Hawaii, Honolulu, HI (MTG, BYH); Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, IA (CFL); Departments of Preventive Medicine (WC) and Pathology (WC, MSS), University of Southern California, Los Angeles, CA; Department of Epidemiology, School of Public Health, Louisiana State University Health Sciences Center, New Orleans, LA (ESP); Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL (EJW); Michigan Department of Community Health, Lansing, MI (GC); Department of Epidemiology, College of Public Health, University of Kentucky, Lexington, KY (CH); Florida Department of Health, Tallahassee, FL (YH); Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD (SFA); Battelle Memorial Institute, Durham, NC (CWL); National Cancer Institute (SA).
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US.
BACKGROUND: 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. METHODS: 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. RESULTS: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. CONCLUSIONS: 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. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US.
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