Investigating a cluster of vulvar cancers in young women: Distribution of human papillomavirus and HPV-16 variants in vulvar dysplastic or neoplastic biopsies

Sarah E. Tan; Suzanne M. Garland; Alice Rumbold; Ibrahim Zardawi; Debbie Taylor-Thomson; John Condon; Sepehr N. Tabrizi

doi:10.1071/SH11179

Investigating a cluster of vulvar cancers in young women: Distribution of human papillomavirus and HPV-16 variants in vulvar dysplastic or neoplastic biopsies

Sarah E. Tan, Suzanne M. Garland, Alice Rumbold, Ibrahim Zardawi, Debbie Taylor-Thomson, John Condon, Sepehr N. Tabrizi

Research output: Contribution to journal › Article › peer-review

Abstract

Background: A high incidence of vulvar cancer, and its precursor lesion,high-grade vulvar intraepithelial neoplasia (VIN) has been identified in youngIndigenous women living in the Arnhem Land region of the Northern Territory(NT) of Australia. This clustering is restricted to women aged <50 years,suggesting that oncogenic human papillomavirus (HPV) is a key causal factor.This study compared the HPV genotype prevalence, HPV-16 variant distributionand p16^INK4aexpression in stored vulvar cancer and high-grade VIN biopsyspecimens from women residing in Arnhem Land, with specimens taken fromIndigenous and non-Indigenous women in other regions of NT where there is noobserved increase in vulvar cancer incidence.

Methods: Twenty high-grade VIN and 10 invasive cancer biopsieswere assessed from Arnhem Land along with 24 high-grade VIN and 10 invasivecancer biopsies from other regions of NT.

Results: Biopsies from Arnhem Land were similar to those fromother regions in the detection of high-risk (HR) or possible HR HPV (VIN: 95%and 84% respectively for Arnhem Land and other regions, P = 0.356; invasive cancer: 100% and 80%, P = 0.473), HPV-16 (VIN: 60% and 80%, P = 0.364; invasive cancer: 70% and 70%, P = 1.0) and p16^INK4a expression(VIN: 90% and 84%, P = 0.673; invasive cancer: 100% and 80%, P = 0.474). All HPV-16 variants were of the Europeanprototype.

Conclusion: Comparison of biopsies revealed no significantdifference in the frequency of oncogenic HPVs or HPV-16 variant types betweenArnhem Land and other regions, suggesting another cofactor in this cluster.

Original language	English
Pages (from-to)	18-25
Number of pages	8
Journal	Sexual Health
Volume	10
Issue number	1
DOIs	https://doi.org/10.1071/SH11179
Publication status	Published - 2013

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@article{33b64cd12feb4b4d9125c83064277190,

title = "Investigating a cluster of vulvar cancers in young women: Distribution of human papillomavirus and HPV-16 variants in vulvar dysplastic or neoplastic biopsies",

abstract = "Background: A high incidence of vulvar cancer, and its precursor lesion,high-grade vulvar intraepithelial neoplasia (VIN) has been identified in youngIndigenous women living in the Arnhem Land region of the Northern Territory(NT) of Australia. This clustering is restricted to women aged <50 years,suggesting that oncogenic human papillomavirus (HPV) is a key causal factor.This study compared the HPV genotype prevalence, HPV-16 variant distributionand p16INK4aexpression in stored vulvar cancer and high-grade VIN biopsyspecimens from women residing in Arnhem Land, with specimens taken fromIndigenous and non-Indigenous women in other regions of NT where there is noobserved increase in vulvar cancer incidence. Methods: Twenty high-grade VIN and 10 invasive cancer biopsieswere assessed from Arnhem Land along with 24 high-grade VIN and 10 invasivecancer biopsies from other regions of NT. Results: Biopsies from Arnhem Land were similar to those fromother regions in the detection of high-risk (HR) or possible HR HPV (VIN: 95%and 84% respectively for Arnhem Land and other regions, P = 0.356; invasive cancer: 100% and 80%, P = 0.473), HPV-16 (VIN: 60% and 80%, P = 0.364; invasive cancer: 70% and 70%, P = 1.0) and p16INK4a expression(VIN: 90% and 84%, P = 0.673; invasive cancer: 100% and 80%, P = 0.474). All HPV-16 variants were of the Europeanprototype. Conclusion: Comparison of biopsies revealed no significantdifference in the frequency of oncogenic HPVs or HPV-16 variant types betweenArnhem Land and other regions, suggesting another cofactor in this cluster.",

keywords = "cyclin dependent kinase inhibitor 2A, article, Australia, cancer incidence, cancer invasion, comparative study, controlled study, female, genotype, geographic distribution, high risk population, human, Human papillomavirus type 16, human tissue, indigenous people, prevalence, protein expression, tumor biopsy, vaginal intraepithelial neoplasia, virus detection, vulva cancer, vulvar intraepithelial neoplasia, Wart virus, Adult, Biopsy, Chi-Square Distribution, Female, Genotype, Human papillomavirus 16, Humans, Middle Aged, Neoplasm Invasiveness, Papillomaviridae, Papillomavirus Infections, Precancerous Conditions, Vulvar Neoplasms",

author = "Tan, {Sarah E.} and Garland, {Suzanne M.} and Alice Rumbold and Ibrahim Zardawi and Debbie Taylor-Thomson and John Condon and Tabrizi, {Sepehr N.}",

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doi = "10.1071/SH11179",

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AU - Tan, Sarah E.

AU - Garland, Suzanne M.

AU - Rumbold, Alice

AU - Zardawi, Ibrahim

AU - Taylor-Thomson, Debbie

AU - Condon, John

AU - Tabrizi, Sepehr N.

PY - 2013

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N2 - Background: A high incidence of vulvar cancer, and its precursor lesion,high-grade vulvar intraepithelial neoplasia (VIN) has been identified in youngIndigenous women living in the Arnhem Land region of the Northern Territory(NT) of Australia. This clustering is restricted to women aged <50 years,suggesting that oncogenic human papillomavirus (HPV) is a key causal factor.This study compared the HPV genotype prevalence, HPV-16 variant distributionand p16INK4aexpression in stored vulvar cancer and high-grade VIN biopsyspecimens from women residing in Arnhem Land, with specimens taken fromIndigenous and non-Indigenous women in other regions of NT where there is noobserved increase in vulvar cancer incidence. Methods: Twenty high-grade VIN and 10 invasive cancer biopsieswere assessed from Arnhem Land along with 24 high-grade VIN and 10 invasivecancer biopsies from other regions of NT. Results: Biopsies from Arnhem Land were similar to those fromother regions in the detection of high-risk (HR) or possible HR HPV (VIN: 95%and 84% respectively for Arnhem Land and other regions, P = 0.356; invasive cancer: 100% and 80%, P = 0.473), HPV-16 (VIN: 60% and 80%, P = 0.364; invasive cancer: 70% and 70%, P = 1.0) and p16INK4a expression(VIN: 90% and 84%, P = 0.673; invasive cancer: 100% and 80%, P = 0.474). All HPV-16 variants were of the Europeanprototype. Conclusion: Comparison of biopsies revealed no significantdifference in the frequency of oncogenic HPVs or HPV-16 variant types betweenArnhem Land and other regions, suggesting another cofactor in this cluster.

AB - Background: A high incidence of vulvar cancer, and its precursor lesion,high-grade vulvar intraepithelial neoplasia (VIN) has been identified in youngIndigenous women living in the Arnhem Land region of the Northern Territory(NT) of Australia. This clustering is restricted to women aged <50 years,suggesting that oncogenic human papillomavirus (HPV) is a key causal factor.This study compared the HPV genotype prevalence, HPV-16 variant distributionand p16INK4aexpression in stored vulvar cancer and high-grade VIN biopsyspecimens from women residing in Arnhem Land, with specimens taken fromIndigenous and non-Indigenous women in other regions of NT where there is noobserved increase in vulvar cancer incidence. Methods: Twenty high-grade VIN and 10 invasive cancer biopsieswere assessed from Arnhem Land along with 24 high-grade VIN and 10 invasivecancer biopsies from other regions of NT. Results: Biopsies from Arnhem Land were similar to those fromother regions in the detection of high-risk (HR) or possible HR HPV (VIN: 95%and 84% respectively for Arnhem Land and other regions, P = 0.356; invasive cancer: 100% and 80%, P = 0.473), HPV-16 (VIN: 60% and 80%, P = 0.364; invasive cancer: 70% and 70%, P = 1.0) and p16INK4a expression(VIN: 90% and 84%, P = 0.673; invasive cancer: 100% and 80%, P = 0.474). All HPV-16 variants were of the Europeanprototype. Conclusion: Comparison of biopsies revealed no significantdifference in the frequency of oncogenic HPVs or HPV-16 variant types betweenArnhem Land and other regions, suggesting another cofactor in this cluster.

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Investigating a cluster of vulvar cancers in young women: Distribution of human papillomavirus and HPV-16 variants in vulvar dysplastic or neoplastic biopsies

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