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FGFR3 mutations in seborrheic keratoses are already present in flat lesions and associated with age and localization
Christian Hafner1, Arndt Hartmann, Johanna M M van Oers
1Department of Dermatology, University of Regensburg, Regensburg, Germany. christian.hafner@klinik.uni-regensburg.de
Abstract:
Somatic activating fibroblast growth factor 3 (FGFR3) mutations in human skin can cause seborrheic keratoses, one of the most frequent skin tumors in man. However, details of the involved mechanisms remain elusive. We analyzed 65 acanthotic seborrheic keratoses with varying vertical diameters for FGFR3 mutations using a SNaPshot multiplex assay. Immunohistochemistry was performed for Ki-67, bcl-2 and FGFR3 protein in all seborrheic keratoses and 19 normal skin samples. FGFR3 mutations were detected in 37 of 65 seborrheic keratoses (57%). These mutations were found both in flat (initial) and thick seborrheic keratoses. FGFR3 mutations were significantly associated with increased age and localization on the head and neck (P<0.01). Ki-67 expression was significantly higher in seborrheic keratoses than in normal epidermis independent of the FGFR3 status (P<0.001). Furthermore, FGFR3 mutations were associated with an increased expression of bcl-2 and FGFR3 protein (P<0.05). Our results indicate that FGFR3 mutations can occur early in the pathogenesis of at least a subset of seborrheic keratoses. Increased age appears to be a risk factor for these mutations. The preferential occurrence of FGFR3 mutations in seborrheic keratoses of the head and neck suggests a causative role for cumulative lifetime ultraviolet light exposure.
Insights
Fibroblast growth factor 3 (FGFR3) mutations are common in seborrheic keratoses, a frequent skin tumor. These mutations, linked to aging and sun exposure, may occur early in tumor development.
Area of Science:
- Dermatology
- Oncology
- Molecular Biology
Background:
- Seborrheic keratoses are common skin tumors.
- Somatic activating fibroblast growth factor 3 (FGFR3) mutations are implicated in their development.
- The precise mechanisms remain unclear.
Purpose of the Study:
- To investigate the prevalence and significance of FGFR3 mutations in seborrheic keratoses.
- To explore the association of FGFR3 mutations with clinicopathological features and protein expression.
Main Methods:
- Analysis of 65 seborrheic keratoses for FGFR3 mutations using SNaPshot multiplex assay.
- Immunohistochemistry for Ki-67, bcl-2, and FGFR3 protein in tumors and normal skin.
- Statistical analysis to correlate mutation status with age, location, and protein expression.
Main Results:
- FGFR3 mutations were detected in 57% of seborrheic keratoses.
- Mutations were associated with increased age and head/neck localization (P<0.01).
- FGFR3 mutations correlated with increased bcl-2 and FGFR3 protein expression (P<0.05).
- Ki-67 expression was higher in seborrheic keratoses than normal epidermis, irrespective of FGFR3 status (P<0.001).
Conclusions:
- FGFR3 mutations can occur early in the pathogenesis of a subset of seborrheic keratoses.
- Increased age is a risk factor for these mutations.
- Head and neck localization suggests a role for cumulative ultraviolet light exposure in FGFR3 mutation development.
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