Vulval squamous cell carcinoma and its precursors

• Published in: Histopathology Vol. 76; no. 1; pp. 128 - 138
• Main Authors: Singh, Naveena, Gilks, C Blake
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.01.2020
• Subjects: Cervix; DEVIL; dVIN; HSIL; Human papillomavirus; Lesions; Pathology; Squamous cell carcinoma; Tumorigenesis; VAAD; VIN; vulva; DEVIL; VAAD; dVIN; VIN; vulva; HSIL; squamous cell carcinoma
• ISSN: 0309-0167; 1365-2559
• DOI: 10.1111/his.13989

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.