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Obstet Gynecol. 2014 Apr;123(4):817-21. doi: 10.1097/AOG.0000000000000171.

Human papillomavirus genotype prevalence in invasive vaginal cancer from a registry-based population.

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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.



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.


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.


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).


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.

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