Differentiated Vulvar Intraepithelial Neoplasia Associated with Intraepithelial Neoplastic Spread
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 18, Issue 3
Abstract
Aims: Differentiated vulvar intraepithelial neoplasia (dVIN) associated with intraepithelial neoplastic spread and with usual vulvar intraepithelial neoplasia (uVIN) has not been studied. Materials and Methods: Consecutive cases of vulvar intraepithelial neoplasia (VIN) diagnosed between 2011-2013 were reviewed. The neoplastic epithelia with or without accompanied invasive squamous cell carcinoma were categorized into: dVIN, uVIN and dVIN associated with scattered atypical neoplastic spread above the parabasal layer in the usual-like VIN pattern (u-like VIN). The lesions were examined with p16 immunostaining. Results: Two- hundred-thirty-five consecutive cases of VIN including 54 invasive squamous cell carcinomas were identified. There were 12 dVIN (invasive, n=8, or 67%), 178 uVIN (invasive, n=5 or 3%) and 45 u-like VIN with or without uVIN (invasive, n=41 or 91%). u-like VIN surface keratinisation exhibited features of keratinizing dysplasia. P16 was immunoreactive in 8%, 69% and 40% of dVIN, uVIN and u-like VIN lesions, respectively. Conclusion: Like dVIN, u-like VIN is commonly associated with invasive squamous cell carcinoma. Therefore, its distinction from uVIN is of pathological and clinical significance.Squamous cell carcinoma (SCC) is the most common cancer of the vulva. It is believed that vulvar invasive SCC, similar to SCC of other body sites, is often preceded by premalignant vulvar intraepithelial lesions (VIN) [1-5]. These lesions are thought to evolve from abnormal basal keratinocytes which, with time, grow upwards to fill the epithelium, accounting for the well-known usual type of VIN (uVIN) . Eventually they acquire the ability to break through the basement membrane and invade into the stroma. This pathway has been best studied in the cervix, but it has also been applied to other squamous /epithelial sites including the bronchus, esophagus and oral cavity [6-8]. uVIN is most often associated with oncogenic HPV. Another distinct pathway towards invasive SCC, found in differentiated vulvar intraepithelial neoplasia (dVIN), involves cytological atypia limited to the basal and parabasal cells. This pathway has been described in the anal canal and anterior oral cavity [9-11]. dVIN lesions are more frequently associated with invasive SCC than uVIN, are often p53 positive by immunohistochemistry, and should be thought of as high grade, despite their subtle histological features [12-14]. dVIN is the type most often associated with untreated or poorly controlled vulvar lichen sclerosus. Since dVIN developed from neoplastic transformation of basal/parabasal cells with early stromal malignant invasion, we hypothesized that there may exist a varying level of upward and intraepithelial spread of dysplastic squamous cells that may mimic uVIN. This study aimed to investigate whether or not the vulvar SCC harbours the above intraepithelial spread, and if present, its clinical and pathological significance. An Immunohistochemical panel consisting of p16, and p53 was also employed as these markers have been shown to distinguish between the differentiated and classic pathways at other sites.Materials and Methods: Ethics approval from the investigational review board of our medical center was obtained. The database at the Department of Anatomical Pathology at the Ottawa Hospital was searched for SCC and vulvar intraepithelial neoplasia diagnosed at our institution between 2011-2013. The patients’ ages were obtained from the pathology reports.
Authors and Affiliations
Kien T Mai, Bojana Djordjevic
Keywords
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- EP ID EP620598
- DOI 10.26717/BJSTR.2019.18.003154
- Views 148
- Downloads 0
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