Reiches (1952) described 7 families in which seborrheic keratosis was transmitted through 2 or 3 generations. The keratoses were of late onset. The skin lesions of the basal cell nevus syndrome sometimes resemble seborrheic keratoses.
Bedi ... Reiches (1952) described 7 families in which seborrheic keratosis was transmitted through 2 or 3 generations. The keratoses were of late onset. The skin lesions of the basal cell nevus syndrome sometimes resemble seborrheic keratoses. Bedi (1977) observed congenital seborrheic verrucae in 11 members in 3 generations of a family.
Logie et al. (2005) screened a series of 62 seborrheic keratoses and found 39% of samples harbored somatic activating FGFR3 mutations (see, e.g., 134934.0005 and 134934.0013) identical to those associated with skeletal dysplasia syndromes and bladder and cervical ... Logie et al. (2005) screened a series of 62 seborrheic keratoses and found 39% of samples harbored somatic activating FGFR3 mutations (see, e.g., 134934.0005 and 134934.0013) identical to those associated with skeletal dysplasia syndromes and bladder and cervical neoplasms. The authors implicated FGFR3 activation as a major cause of benign epidermal tumors in humans. Hafner et al. (2007) identified heterozygous somatic mutations in the PIK3CA gene (see, e.g., 171834.0001 and 171834.0003) in 10 (16%) of 62 seborrheic keratosis lesions. Three of the lesions had concomitant somatic mutations in the FGFR3 gene (see, e.g., R248C; 134934.0005). Histologic analysis identified 8 acanthotic lesions, 1 hyperkeratotic lesion, and 1 adenoid lesion. In 3 patients, multiple individual lesions were analyzed. In 2 patients, all lesions had wildtype PIK3CA and FGFR3 genes, whereas in the third case, 1 lesion had a mutation, and 7 other lesions had wildtype sequences. The findings suggested that, in addition to their role in cancer, oncogenic PIK3CA mutations contribute to the pathogenesis of skin tumors lacking malignant potential.