Sign up for Table of Contents Alerts.
Email this page
Print this page
Perspectives
FGFR3 Mutations in Benign Skin Tumors
Christian Hafner, Thomas Vogt and Arndt Hartmann
volume 5 | issue 23
1 december 2006Pages: 2723 - 2728
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
Activating FGFR3 germline mutations cause skeletal dysplasia and craniosynostosis syndromes. Somatic FGFR3 mutations have been identified in several cancer entities such as urothelial carcinoma and multiple myeloma. Recently, the same FGFR3 mutations known from skeletal dysplasia syndromes and urothelial carcinoma have been shown to cause benign human skin tumors such as seborrheic keratoses and epidermal nevi. The underlying mechanisms for the somatic FGFR3 mutations in the epidermis are unknown so far, as well as details of the involved signaling pathways in the mutant keratinocytes leading to the formation of acanthotic skin tumors. Herein we discuss potential mechanisms and functional consequences of activating FGFR3 mutations in human skin. Further studies are required to provide insights in the pathogenesis of benign skin tumors caused by FGFR3 mutations. These studies will add to new non-invasive therapeutical strategies for benign acanthotic skin tumors in dermatology.
Authors
Christian Hafner
University of Regensburg; Regensburg Germany
Thomas Vogt
University of Regensburg; Regensburg Germany
Arndt Hartmann
University of Regensburg; Regensburg Germany
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.