Additional research is needed to further establish possible etiological risk factors and to clarify the involvement of PIK3CA and FGFR3 genes in the pathogenesis of seborrheic keratosis of the outer ear canal.
We performed a comprehensive mutational screen of genes in the FGFR3-RAS-MAPK and phosphoinositide 3-kinase (PI3K)-AKT pathways from 175 SK, including multiple lesions from each patient.
Because FGFR3 and PIK3CA mutations have been reported to be involved in the pathogenesis of seborrhoeic keratosis, we analysed whether these mutations are also present in STK and DPN.
Because FGFR3 and PIK3CA mutations have been reported to be involved in the pathogenesis of sporadic SK, we analysed five SKs of an affected family member for hotspot mutations of these genes.
Somatic oncogenic activating mutations in FGFR3 and/or PIK3CA have recently been described in benign epithelial cutaneous lesions that never progress to malignancy (seborrheic keratoses and epidermal nevi).