SOX2 Expression in Vulvar Squamous Epithelial Neoplastic Lesions: Relation with the Antiapoptotic Factor Survivin
Hermann Brustmann. Landesklinikum Baden-Moedling, Moedling, Lower Austria, Austria
Background: SOX2 is a transcription factor that controls pluripotency in both embryonic and adult-tissue stem cells. Survivin is involved in the regulation of the cell cycle progression and a potent inhibitor of apoptosis. These factors are overexpressed in many cancers including squamous cell carcinomas and their precursor lesions, with a role of SOX2 as a cell lineage-survival oncogene in the latter tumors.
Design: SOX2 and survivin immunoexpression was evaluated in formalin-fixed, paraffin-embedded archival vulvar epithelia consisting of normal squamous vulvar epithelia (NE, n=25), high-grade classic vulvar intraepithelial neoplasia (HG-VIN, n=16), differentiated VIN (d-VIN, n=18) and vulvar invasive keratinizing squamous cell carcinoma (ISCC, n=33). Immunostaining for all factors was scored for quantity (score 0, 0% immunoreactive cells; score 1+, <5% immunoreactive cells; score 2+, 5% to 50% immunoreactive cells; score 3+, >50% immunoreactive cells) and intensity (scores 1+, 2+, 3+). These scores were added in the individual cases to achieve the final immunoscores. Final scores of 0 and 1+ were considered negative, scores 2 to 4 as moderately and scores 5 and 6 as strongly positive.
Results: Moderate and strong immunoexpression of SOX2 and survivin was noted in neoplastic lesions only. Immunoscores did not differ significantly in HG-VIN and ISCC (P=0.732, and 0.097, respectively) and in grades 1, 2 and 3 of ISCC, indicating a correlation of these factors. In d-VIN, SOX2 was upregulated as compared to survivin (P=0.003).
Conclusions: SOX2 and survivin are up-regulated and correlated in HG-VIN and ISCC compared to non-neoplastic squamous epithelia indicating relevance to vulvar carcinogenesis, consistent with the function of SOX2 as a cell lineage-survival oncogene and of survivin activation in the development of cellular longevity and resistance to apoptosis. A lack of a correlation in d-VIN points towards different marker biology in preinvasive intraepithelial lesions of different pathways.
Category: Gynecologic & Obstetrics
Tuesday, March 5, 2013 1:00 PM
Poster Session IV # 235, Tuesday Afternoon