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Author Notes:

Corresponding Author: Mona Saraiya, MD, MPH, Mona Saraiya, 4770 Buford Hwy, Mailstop K76, Atlanta, GA 30341, 770-488-4226, msaraiya@cdc.gov

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


Research Funding:

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 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 NPCR registries; and genotyping were largely supported by 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.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Obstetrics & Gynecology
  • DNA
  • HPV

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

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Journal Title:



Volume 123, Number 4


, Pages 817-821

Type of Work:

Article | Post-print: After Peer Review


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% (P5.038). 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) (P5.003). 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 (P5.243). 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.

Copyright information:

© 2014 by The American College of Obstetricians and Gynecologists.

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