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Human Papillomavirus Genotype Prevalence in Invasive Vaginal Cancer From a Registry-Based Population

Sinno, Abdulrahman K. MD; Saraiya, Mona MD, MPH; Thompson, Trevor D. BS; Hernandez, Brenda Y. PhD, MPH; Goodman, Marc T. PhD, MPH; Steinau, Martin PhD; Lynch, Charles F. PhD, MD; Cozen, Wendy DO, MPH; Saber, Maria Sibug MD; Peters, Edward S. ScD, DMD; Wilkinson, Edward J. MD; Copeland, Glenn MBA; Hopenhayn, Claudia PhD, MPH; Watson, Meg MPH; Lyu, Christopher MPA; Unger, Elizabeth R. PhD, MD

doi: 10.1097/AOG.0000000000000171
Contents: Original Research

OBJECTIVE: To describe the human papillomavirus (HPV) genotype distribution in invasive vaginal cancers diagnosed before the introduction of the HPV vaccine and evaluate if survival differed by HPV status.

METHODS: Four population-based registries and three residual tissue repositories provided formalin-fixed, paraffin-embedded tissue from microscopically confirmed primary vaginal cancer cases diagnosed between 1994 and 2005 that were tested by L1 consensus polymerase chain reaction with type-specific hybridization in a central laboratory. Clinical, demographic, and all-cause survival data were assessed by HPV status.

RESULTS: Sixty cases of invasive vaginal cancer were included. Human papillomavirus was detected in 75% (45) and 25% (15) were HPV-negative. HPV 16 was most frequently detected (55% [33/60]) followed by HPV 33 (18.3% [11/60]). Only one case was positive for HPV 18 (1.7%) Multiple types were detected in 15% of the cases. Vaginal cancers in women younger than 60 years were more likely to be HPV 16– or HPV 18–positive (HPV 16 and 18) than older women, 77.3% compared with 44.7% (P=.038). The median age at diagnosis was younger in the HPV 16 and 18 (59 years) group compared with other HPV-positive (68 years) and no HPV (77 years) (P=.003). The HPV distribution did not significantly vary by race or ethnicity or place of residence. The 5-year unadjusted all-cause survival was 57.4% for women with HPV-positive vaginal cancers compared with 35.7% among those with HPV-negative tumors (P=.243).

CONCLUSION: Three fourths of all vaginal cancers in the United States had HPV detected, much higher than previously found, and 57% could be prevented by current HPV vaccines.


Human papillomavirus (HPV) 16 and 33, not HPV 18, are the most prevalent HPV types found in invasive vaginal cancers from a multicenter registry-based U.S. population of 60 patients.

Kelly Gynecologic Oncology Service, Department of Gynecology and Obstetrics, Johns Hopkins University, Baltimore, Maryland; the Division of Gynecologic Oncology, Emory University, Department of Gynecology and Obstetrics, and the Division of Cancer Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, and the Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; the University of Hawaii Cancer Center, University of Hawaii, Honolulu, Hawaii; the Department of Epidemiology, College of Public Health, The University of Iowa, Iowa City, Iowa; the Norris Comprehensive Cancer Center and Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California; the Department of Epidemiology, School of Public Health, Louisiana State University Health Sciences Center, New Orleans, Louisiana; the Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, and the Florida Department of Health, Tallahassee, Florida; the Michigan Department of Community Health, Lansing, Michigan; the Department of Epidemiology, College of Public Health, University of Kentucky, Lexington, Kentucky; and the Battelle Memorial Institute, Durham, North Carolina.

Corresponding author: Mona Saraiya, MD, MPH, Mona Saraiya, 4770 Buford Highway, Mailstop K76, Atlanta, GA 30341; e-mail:

Supported in part by the Centers for Disease Control and Prevention grants NO. 5U58DP000810-5 (Kentucky), 5U58DP000844-5 (Florida), 5U58DP000812-5 (Michigan), and 5U58DP000769-5 (Louisiana) and from the Surveillance, Epidemiology, and End Results (SEER) Program, National Institutes of Health,

Department of Health and Human Services under Contracts N01-PC-35139 (Los Angeles), N01-PC-35143 (Iowa), and N01-PC-35137 (Hawaii). The support for collection of specimens from Kentucky, Florida, Michigan, and Louisiana coordination of genotyping data from both SEER and National Program for Cancer Registries and genotyping were largely supported by the Centers for Disease Control and Prevention (CDC) intramural funds and Vaccine for Children Funds. The collection of data from California was largely supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; by the National Cancer Institute, National Institutes of Health, Department of Health and Human Services under Contract N01-PC-2010-00035; and grant number 1U58DP000807-3 from the CDC.

The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the CDC.

Financial Disclosure Dr. Hernandez has received consultation and speaker fees from Merck and Co, Inc. The other authors did not report any potential conflicts of interest.

© 2014 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.