Objective: Vulvar cancer is a rare malignancy, representing approximately 5% of all female genital tract cancers and 1% of all malignancies in women. The incidence of vulvar carcinoma in situ (VIN III) has nearly doubled from 1.1 to 2.1 per 100,000 women-years between 1973 and 1987. It is more frequent among older women, but the incidence is increasing among younger women. Different factors have been associated with an increased risk for vulvar cancers, for example HPV and genital infection. In this study we investigated normal, preinvasive and invasive vulvar tissues to look for relevant changes of Tenascin, a glycoprotein, already detected in pre-invasive and invasive lesions of the breast.
Materials and methods: Paraffin-embedded slides from 15 normal vulvar tissue, 14 cases of vulvar cancer, 51 cases of VIN (12 VIN I, 18 VIN II, 21 VIN III) and 5 cases of vulvar vestibulitis were investigated with immunofluorescent microscopical methods.
Results: Tenascin was detectable and clearly enhanced in the stroma underlying the basement membrane in all samples of patients with VIN. The stroma of all specimens of patients with vulvar cancers showed intensive and strong reactivity. No Tenascin expression was observed in normal human vulvar skin. Tenascin expression also markedly increased in tissue lesions with skin inflammation. Tissue samples presenting vulvar intraepithelial neoplasia showed different intensity of staining, with a higher grade of VIN resulting in more immunohistochemical reactivity.
Conclusion: Our findings indicate the potential role of Tenascin staining as a marker of malignancy and a predictor of invasiveness in vulvar intraepithelial neoplasia. The preponderance of these lesions has been noted in an increasingly younger population (median age: 50 years). Tenascin was detectable in inflammatory vulvar disease, preinvasive and invasive vulvar lesions, but not in normal vulvar tissue. The enhancement of Tenascin in vulvar premalignant and malignant disease seems to be of inflammatory origin.