Investigating a cluster of vulvar cancer in young women

a cross-sectional study of genital human papillomavirus prevalence

Alice Rumbold, Sarah Tan, John Condon, Debbie Taylor-Thomson, Maria Nickels, Sepehr Tabrizi, M Davy, M O'Brien, Christine Connors, I Zardawi, Jim Stankovich, Suzanne Garland

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Abstract

Background: Vulvar cancer is a relatively rare malignancy, which occurs most often in postmenopausal women. We have previously identified a geographic cluster of vulvar cancer in young Indigenous women living in remote communities in the Arnhem Land region of Australia. In this population, we investigated the prevalence of oncogenic human papillomavirus (HPV) infection in anogenital samples (vulvar/vaginal/perianal area and cervix) and compared the overall, type-specific and multiple infection prevalence between sites.

Methods: A cross-sectional survey of 551 Indigenous women aged 18-60 years was undertaken in 9 Arnhem Land communities. Women were consented for HPV detection and genotyping collected by a combined vulvar/vaginal/perianal (VVP) sweep swab and a separate PreservCyt endocervical sample collected during Pap cytology screening. HPV DNA testing was undertaken using PCR with broad spectrum L1 consensus PGMY09/11 primers with genotyping of positive samples by Roche Linear Array. The primary outcomes were the prevalence of cervical and VVP high-risk (HR) HPV.

Results: The prevalence of VVP HR-HPV was 39%, which was significantly higher than the cervical HR-HPV prevalence (26%, p<0.0001). HPV-16 was the most common genotype detected in both sites (VVP 11%, cervical 6%). HPV-16 infection peaked in women aged <20 years; however, there was a marked decline in cervical HPV-16 prevalence with age (p=0.007), whereas following an initial decline, the prevalence of VVP HPV-16 remained constant in subsequent age-groups (p=0.835).

Conclusions: In this population experiencing a cluster of vulvar cancer, the prevalence of cervical oncogenic HPV infection was similar to that reported by studies of other Australian women; however there was a significantly higher prevalence of vulvar/vaginal/perianal infection to cervical. The large discrepancy in HPV prevalence between anogenital sites in this population may represent more persistent infection at the vulva. This needs further investigation, including the presence of possible environmental and/or genetic factors that may impair host immunity.
Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalBMC Infectious Diseases
Volume12
DOIs
Publication statusPublished - 2012

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Vulvar Neoplasms
Cross-Sectional Studies
Human papillomavirus 16
Papillomavirus Infections
Infection
Population
Vulva
Cervix Uteri
Cell Biology
Immunity
Age Groups
Genotype

Cite this

Rumbold, Alice ; Tan, Sarah ; Condon, John ; Taylor-Thomson, Debbie ; Nickels, Maria ; Tabrizi, Sepehr ; Davy, M ; O'Brien, M ; Connors, Christine ; Zardawi, I ; Stankovich, Jim ; Garland, Suzanne. / Investigating a cluster of vulvar cancer in young women : a cross-sectional study of genital human papillomavirus prevalence. In: BMC Infectious Diseases. 2012 ; Vol. 12. pp. 1-8.
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title = "Investigating a cluster of vulvar cancer in young women: a cross-sectional study of genital human papillomavirus prevalence",
abstract = "Background: Vulvar cancer is a relatively rare malignancy, which occurs most often in postmenopausal women. We have previously identified a geographic cluster of vulvar cancer in young Indigenous women living in remote communities in the Arnhem Land region of Australia. In this population, we investigated the prevalence of oncogenic human papillomavirus (HPV) infection in anogenital samples (vulvar/vaginal/perianal area and cervix) and compared the overall, type-specific and multiple infection prevalence between sites.Methods: A cross-sectional survey of 551 Indigenous women aged 18-60 years was undertaken in 9 Arnhem Land communities. Women were consented for HPV detection and genotyping collected by a combined vulvar/vaginal/perianal (VVP) sweep swab and a separate PreservCyt endocervical sample collected during Pap cytology screening. HPV DNA testing was undertaken using PCR with broad spectrum L1 consensus PGMY09/11 primers with genotyping of positive samples by Roche Linear Array. The primary outcomes were the prevalence of cervical and VVP high-risk (HR) HPV.Results: The prevalence of VVP HR-HPV was 39{\%}, which was significantly higher than the cervical HR-HPV prevalence (26{\%}, p<0.0001). HPV-16 was the most common genotype detected in both sites (VVP 11{\%}, cervical 6{\%}). HPV-16 infection peaked in women aged <20 years; however, there was a marked decline in cervical HPV-16 prevalence with age (p=0.007), whereas following an initial decline, the prevalence of VVP HPV-16 remained constant in subsequent age-groups (p=0.835).Conclusions: In this population experiencing a cluster of vulvar cancer, the prevalence of cervical oncogenic HPV infection was similar to that reported by studies of other Australian women; however there was a significantly higher prevalence of vulvar/vaginal/perianal infection to cervical. The large discrepancy in HPV prevalence between anogenital sites in this population may represent more persistent infection at the vulva. This needs further investigation, including the presence of possible environmental and/or genetic factors that may impair host immunity.",
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author = "Alice Rumbold and Sarah Tan and John Condon and Debbie Taylor-Thomson and Maria Nickels and Sepehr Tabrizi and M Davy and M O'Brien and Christine Connors and I Zardawi and Jim Stankovich and Suzanne Garland",
year = "2012",
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Rumbold, A, Tan, S, Condon, J, Taylor-Thomson, D, Nickels, M, Tabrizi, S, Davy, M, O'Brien, M, Connors, C, Zardawi, I, Stankovich, J & Garland, S 2012, 'Investigating a cluster of vulvar cancer in young women: a cross-sectional study of genital human papillomavirus prevalence', BMC Infectious Diseases, vol. 12, pp. 1-8. https://doi.org/10.1186/1471-2334-12-243

Investigating a cluster of vulvar cancer in young women : a cross-sectional study of genital human papillomavirus prevalence. / Rumbold, Alice; Tan, Sarah; Condon, John; Taylor-Thomson, Debbie; Nickels, Maria; Tabrizi, Sepehr; Davy, M; O'Brien, M; Connors, Christine; Zardawi, I; Stankovich, Jim; Garland, Suzanne.

In: BMC Infectious Diseases, Vol. 12, 2012, p. 1-8.

Research output: Contribution to journalArticleResearchpeer-review

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T1 - Investigating a cluster of vulvar cancer in young women

T2 - a cross-sectional study of genital human papillomavirus prevalence

AU - Rumbold, Alice

AU - Tan, Sarah

AU - Condon, John

AU - Taylor-Thomson, Debbie

AU - Nickels, Maria

AU - Tabrizi, Sepehr

AU - Davy, M

AU - O'Brien, M

AU - Connors, Christine

AU - Zardawi, I

AU - Stankovich, Jim

AU - Garland, Suzanne

PY - 2012

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N2 - Background: Vulvar cancer is a relatively rare malignancy, which occurs most often in postmenopausal women. We have previously identified a geographic cluster of vulvar cancer in young Indigenous women living in remote communities in the Arnhem Land region of Australia. In this population, we investigated the prevalence of oncogenic human papillomavirus (HPV) infection in anogenital samples (vulvar/vaginal/perianal area and cervix) and compared the overall, type-specific and multiple infection prevalence between sites.Methods: A cross-sectional survey of 551 Indigenous women aged 18-60 years was undertaken in 9 Arnhem Land communities. Women were consented for HPV detection and genotyping collected by a combined vulvar/vaginal/perianal (VVP) sweep swab and a separate PreservCyt endocervical sample collected during Pap cytology screening. HPV DNA testing was undertaken using PCR with broad spectrum L1 consensus PGMY09/11 primers with genotyping of positive samples by Roche Linear Array. The primary outcomes were the prevalence of cervical and VVP high-risk (HR) HPV.Results: The prevalence of VVP HR-HPV was 39%, which was significantly higher than the cervical HR-HPV prevalence (26%, p<0.0001). HPV-16 was the most common genotype detected in both sites (VVP 11%, cervical 6%). HPV-16 infection peaked in women aged <20 years; however, there was a marked decline in cervical HPV-16 prevalence with age (p=0.007), whereas following an initial decline, the prevalence of VVP HPV-16 remained constant in subsequent age-groups (p=0.835).Conclusions: In this population experiencing a cluster of vulvar cancer, the prevalence of cervical oncogenic HPV infection was similar to that reported by studies of other Australian women; however there was a significantly higher prevalence of vulvar/vaginal/perianal infection to cervical. The large discrepancy in HPV prevalence between anogenital sites in this population may represent more persistent infection at the vulva. This needs further investigation, including the presence of possible environmental and/or genetic factors that may impair host immunity.

AB - Background: Vulvar cancer is a relatively rare malignancy, which occurs most often in postmenopausal women. We have previously identified a geographic cluster of vulvar cancer in young Indigenous women living in remote communities in the Arnhem Land region of Australia. In this population, we investigated the prevalence of oncogenic human papillomavirus (HPV) infection in anogenital samples (vulvar/vaginal/perianal area and cervix) and compared the overall, type-specific and multiple infection prevalence between sites.Methods: A cross-sectional survey of 551 Indigenous women aged 18-60 years was undertaken in 9 Arnhem Land communities. Women were consented for HPV detection and genotyping collected by a combined vulvar/vaginal/perianal (VVP) sweep swab and a separate PreservCyt endocervical sample collected during Pap cytology screening. HPV DNA testing was undertaken using PCR with broad spectrum L1 consensus PGMY09/11 primers with genotyping of positive samples by Roche Linear Array. The primary outcomes were the prevalence of cervical and VVP high-risk (HR) HPV.Results: The prevalence of VVP HR-HPV was 39%, which was significantly higher than the cervical HR-HPV prevalence (26%, p<0.0001). HPV-16 was the most common genotype detected in both sites (VVP 11%, cervical 6%). HPV-16 infection peaked in women aged <20 years; however, there was a marked decline in cervical HPV-16 prevalence with age (p=0.007), whereas following an initial decline, the prevalence of VVP HPV-16 remained constant in subsequent age-groups (p=0.835).Conclusions: In this population experiencing a cluster of vulvar cancer, the prevalence of cervical oncogenic HPV infection was similar to that reported by studies of other Australian women; however there was a significantly higher prevalence of vulvar/vaginal/perianal infection to cervical. The large discrepancy in HPV prevalence between anogenital sites in this population may represent more persistent infection at the vulva. This needs further investigation, including the presence of possible environmental and/or genetic factors that may impair host immunity.

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