Epithelial Induction in Dermatofibroma: A Role for the Epidermal Growth Factor (EGF) Receptor

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Abstract
Dermatofibroma (DF) refers to a spectrum of firm, nodular, nonencapsulated lesions that occur commonly on the extremities. Histologically, DF is composed of spindle cells with variable differentiation toward histiocytic and vascular elements, often associated with epithelial hyperplasia and basilar keratinocyte pigmentation that histologically may simulate basal cell carcinoma (BCC). The characteristic epithelial changes are likely to be mesenchyma-mediated and probably represent a host reparative response otherwise known as the inductive phenomenon. Epidermal-mesenchymal cellular interactions, including induction, occur in various stages of embryonic skin development and in response to injury with tissue repair. Cellular interaction is mediated by direct apposition of cells or by soluble protein hormones produced directly by the cell (autocrine effect) or adjacent cells (paracrine effect). Among the important soluble mediators are epidermal growth factor (EGF), which is known to stimulate the proliferation and differentiation of a variety of transformed and benign tissues. We investigated the possible etiologic association between EGF receptor (EGF-R) expression and epithelial induction in a prospective series of 20 cases of DF compared to entities such as granular cell tumor, scar tissue, and nevus sebaceus similarly showing epithelial hyperplasia. Immunohistochemical staining for EGF-R showed strong dermal staining of dendritic spindle cells and overlying hyperplastic keratinocytes in each of the DF cases. Immunohistochemical staining for EGF-R was absent within all dermal loci of granular cell tumor (n = 3), nevus sebaceus (n = 6), and scar tissue (n = 12).