Human papillomavirus type-distribution in vulvar and vaginal cancers and their associated precursors.
OBJECTIVE
Data on human papillomavirus (HPV) prevalence in vulvar and vaginal cancers are limited. These data are important to predict the potential future effect of prophylactic HPV vaccines. Our aim was to conduct a systematic review of HPV type distribution in vulvar and vaginal invasive carcinomas, vulvar intraepithelial neoplasia (VIN), and vaginal intraepithelial neoplasia.


METHODS
A MEDLINE search was conducted using the terms vulvar/vaginal cancer, intraepithelial neoplasia, and HPV/human papillomavirus through September 2007 with no specified start date or language restrictions.


METHODS
A total of 725 abstracts (564 vulvar, 161 vaginal) were reviewed, of which 67 studies (56 vulvar, 11 vaginal) met the inclusion criteria of using polymerase chain reaction (PCR) or hybrid capture assays for HPV DNA detection and having more than one case with HPV data available.


RESULTS
This review identified 2,790 vulvar (1,379 invasive, 1,340 VIN2/3, 71 VIN1) and 315 vaginal cases (83 invasive, 166 vaginal intraepithelial neoplasia 2/3, 66 vaginal intraepithelial neoplasia 1). Most cases were from North America and Europe (87.2%), with few from Asia (5.5%) and South America (7.3%). Human papillomavirus prevalence in vulvar cancer, VIN2/3, and VIN1 was 40.1%, 80.4%, and 77.5%, respectively. HPV prevalence in vaginal cancer, vaginal intraepithelial neoplasia (VAIN)2/3, and VAIN1 was relatively higher at 65.5%, 92.6%, and 98.5%, respectively. HPV16 was the most common type in vulvar (29.3%) and vaginal (55.4%) cancers, VIN2/3 (71.2%) and VAIN2/3 (65.8%).


CONCLUSIONS
Human papillomavirus prevalence was higher among vaginal than vulvar cases, and HPV16 accounted for most HPV-positive cases for both cancers. Although the potential effect of HPV vaccines on these gynecologic cancers may not be as high as for cervical cancer due to their more diverse causes, vaccinating young women against HPV16/18 may help to reduce the incidence of HPV-related cases.
Smith
Jennifer S
JS
From the Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina; Departments of Pathology, Gynecology, and Obstetrics, Johns Hopkins Medical Institutions, Baltimore, Maryland; and Worldwide Epidemiology, GlaxoSmithKline, Greenford, Middlesex, United Kingdom.
Backes
Danielle M
DM
Hoots
Brooke E
BE
Kurman
Robert J
RJ
Pimenta
Jeanne M
JM
D004279:DNA, Viral / Q000737:chemistry / Q000235:genetics; D005260:Female; D052162:Human papillomavirus 16 / Q000302:isolation & purification / Q000472:pathogenicity; D006801:Humans; D027383:Papillomaviridae / Q000302:isolation & purification*; D030361:Papillomavirus Infections / Q000150:complications / Q000453:epidemiology* / Q000517:prevention & control*; D053918:Papillomavirus Vaccines / Q000008:administration & dosage*; D015995:Prevalence; D002583:Uterine Cervical Neoplasms / Q000453:epidemiology / Q000473:pathology / Q000821:virology*; D014625:Vaginal Neoplasms / Q000453:epidemiology / Q000473:pathology / Q000821:virology*; D014846:Vulvar Neoplasms / Q000453:epidemiology / Q000473:pathology / Q000821:virology*
D004279:DNA, Viral; D053918:Papillomavirus Vaccines