Abstract
Seborrheic keratosis (SK) and epidermal nevi (EN) represent benign skin tumors and congenital lesions, respectively. Oncogenic mutations are fundamentally involved in their pathogenesis and SK is characterized by a broad spectrum of somatic mutations in the FGFR3, PIK3CA, RAS, AKT1 and EGFR genes. In contrast to malignant tumors, SK is genetically stable without alterations of tumor suppressor genes. The ENs are caused by postzygotic activating hot spot mutations in FGFR3, PIK3CA and particularly HRAS, resulting in a genetic mosaicism. The size of the lesions and the differentiation potential of the mutated cell into various tissue types depends on the time point of the mutation during embryogenesis. The genetic mosaic may predispose to a later growth of benign and malignant (adnexal) tumors.
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