Epidermal growth factor receptor is involved in the development of an invasive phenotype in vulvar squamous lesions, but is not related to MIB-1 immunoreactivity.

This study investigated the expression of epidermal growth factor receptor (EGFR) and proliferation as determined by MIB-1 labeling indices (proliferation index [PI]) in 82 cases of vulvar tissues consisting of healthy epithelia (HE) (n = 10), vulvar condylomas (VC; n = 24), high-grade vulvar intraepithelial neoplasias (HG-VIN) of warty and basaloid types (n = 26), invasive keratinizing squamous cell carcinomas (SCCs; n = 22), and differentiated VIN adjacent to SCCs (n = 7) by means of a standard immunohistochemical method using monoclonal antibodies to characterize EGFR expression, with an emphasis on neoplastic transformation and progression, and to relate it to proliferation. The EGFR expression was mainly membranous and--to a lesser degree--cytoplasmic; it was scored for intensity and quantity. The MIB-1 reactivity was exclusively nuclear. High EGFR immunoscores were detected on 6% of HG-VIN and 41% of SCCs. The EGFR immunoexpression increased significantly from healthy epithelia to VCs, VINs (HG-VIN and differentiated VIN taken together), and SCCs (P < 0.0001 [chi2 test]), but was not related to stage, grade, or recurrence in SCCs. There was no statistical significance for EGFR immunoscores and PIs in the groups of VCs (P = 0.1923), VINs (P = 0.0951), and SCCs (P = 0.6896). This study shows the upregulation of EGFR expression in a few warty and basaloid HG-VIN cases and in many SCCs of the vulva. The lack of a relationship with PIs suggests that mechanisms other than proliferation are involved in this process.