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 in | Histopathology Vol. 76; no. 1; pp. 128 - 138 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
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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. |
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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 givenname: Naveena orcidid: 0000-0003-1782-1967 surname: Singh fullname: Singh, Naveena organization: Queen Mary University of London – sequence: 2 givenname: C Blake orcidid: 0000-0001-7889-8250 surname: Gilks fullname: Gilks, C Blake email: blake.gilks@vch.ca organization: Vancouver General Hospital |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31846523$$D View this record in MEDLINE/PubMed |
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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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SubjectTerms | Cervix DEVIL dVIN HSIL Human papillomavirus Lesions Pathology Squamous cell carcinoma Tumorigenesis VAAD VIN vulva |
Title | Vulval squamous cell carcinoma and its precursors |
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