Vulval squamous cell carcinoma and its precursors

Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)‐associated and HPV‐independent], and these VSCC variants are recognised as different disease entities on the basis of different aetiologies, morphological features, molecular events during oncog...

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Published inHistopathology Vol. 76; no. 1; pp. 128 - 138
Main Authors Singh, Naveena, Gilks, C Blake
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.01.2020
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Abstract Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)‐associated and HPV‐independent], and these VSCC variants are recognised as different disease entities on the basis of different aetiologies, morphological features, molecular events during oncogenesis, precursor lesions, prognosis, and response to treatment. The precursor of HPV‐associated VSCC, variously referred to as high‐grade squamous intraepithelial lesion (HSIL) [vulvar intraepithelial neoplasia (VIN) 2/3] or usual‐type VIN, is morphologically identical to the more common HSIL (cervical intraepithelial neoplasia 2/3) of the cervix. The precursor lesions of HPV‐independent VSCC include differentiated VIN, differentiated exophytic vulvar intraepithelial lesion, and vulvar acanthosis with altered differentiation; these have been under‐recognised by pathologists in the past, leading to delays in treatment. This review will discuss the recent advances in diagnostic surgical pathology of VSCC and its precursors, and how these diagnoses can impact on patient management.
AbstractList Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)‐associated and HPV‐independent], and these VSCC variants are recognised as different disease entities on the basis of different aetiologies, morphological features, molecular events during oncogenesis, precursor lesions, prognosis, and response to treatment. The precursor of HPV‐associated VSCC, variously referred to as high‐grade squamous intraepithelial lesion (HSIL) [vulvar intraepithelial neoplasia (VIN) 2/3] or usual‐type VIN, is morphologically identical to the more common HSIL (cervical intraepithelial neoplasia 2/3) of the cervix. The precursor lesions of HPV‐independent VSCC include differentiated VIN, differentiated exophytic vulvar intraepithelial lesion, and vulvar acanthosis with altered differentiation; these have been under‐recognised by pathologists in the past, leading to delays in treatment. This review will discuss the recent advances in diagnostic surgical pathology of VSCC and its precursors, and how these diagnoses can impact on patient management.
Author Singh, Naveena
Gilks, C Blake
Author_xml – sequence: 1
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  orcidid: 0000-0003-1782-1967
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  surname: Gilks
  fullname: Gilks, C Blake
  email: blake.gilks@vch.ca
  organization: Vancouver General Hospital
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Keywords DEVIL
VAAD
dVIN
VIN
vulva
HSIL
squamous cell carcinoma
Language English
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Snippet Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)‐associated and HPV‐independent], and these VSCC...
Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)-associated and HPV-independent], and these VSCC...
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StartPage 128
SubjectTerms Cervix
DEVIL
dVIN
HSIL
Human papillomavirus
Lesions
Pathology
Squamous cell carcinoma
Tumorigenesis
VAAD
VIN
vulva
Title Vulval squamous cell carcinoma and its precursors
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fhis.13989
https://www.ncbi.nlm.nih.gov/pubmed/31846523
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