Hafner, C. and Hafner, H. and Groesser, L. (2014) Genetic basis of seborrheic keratosis and epidermal nevi. PATHOLOGE, 35 (5). 413-+. ISSN 0172-8113, 1432-1963
Full text not available from this repository. (Request a copy)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.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | GROWTH-FACTOR RECEPTOR-3; ACTIVATING FGFR3 MUTATIONS; BENIGN SKIN TUMORS; PIK3CA MUTATIONS; RAS MUTATIONS; HRAS MUTATION; PHAKOMATOSIS PIGMENTOKERATOTICA; THANATOPHORIC DYSPLASIA; POSTZYGOTIC HRAS; KRAS MUTATIONS; Oncogenic mutations; Hot spot mutations; Genetic mosaic; Congenital malformations; Adnexal tumors |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Dermatologie und Venerologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 28 Aug 2019 08:57 |
| Last Modified: | 28 Aug 2019 08:57 |
| URI: | https://pred.uni-regensburg.de/id/eprint/9657 |
Actions (login required)
 |
View Item |
