Journal
INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER
Volume 21, Issue 7, Pages 1297-1305Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/IGC.0b013e31822dbe26
Keywords
Differentiated; Vulval intraepithelial neoplasia; Cancer; Vulva; Squamous; Etiology; Carcinogenesis; Hyperplasia
Categories
Funding
- Griffiths Gynaecology Special Purpose Fund
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Vulval squamous cell carcinoma appears to arise via 2 distinct pathways. A significant minority are associated with oncogenic human papillomavirus (HPV) infection and undifferentiated vulval intraepithelial neoplasia (VIN). However, the majority arises in the absence of HPV, on a background of chronic inflammation. Until recently, it was assumed that lichen sclerosus was the underlying inflammatory condition in the majority of HPV-negative cancers. This pathway of carcinogenesis has been less well studied than the HPV pathway. Emerging evidence implicates differentiated VIN (DVIN), rather than lichen sclerosus, as the most likely precursor lesion in HPV-negative vulval squamous cell carcinoma. Here we discuss the clinical and molecular evidence that implicates DVIN as a lesion with a high malignant potential. This lesion is probably underdiagnosed and may be undertreated. Better recognition of DVIN by gynecologists and pathologists may therefore offer an opportunity to prevent some vulval cancers.
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