1. Home>
2. Specialties>
3. Dermatology>
4. Summary and Comment

Oncogenic Lesions in Lentigines

Researchers establish a genetic link between keratoses and lentigines, but not all mutations lead to cancer.

Solar lentigines (SLs) and reticulated seborrheic keratoses (SKs) share similar pathological features, and their clinical appearance often overlaps. Recent identification of somatic mutations of the fibroblast growth factor receptor gene FGFR3 and the PIK3CA gene in SKs suggests that SLs may harbor similar oncogenic lesions. Investigators in Germany analyzed DNA from 30 SLs in 29 patients for common oncogenic mutations in FGFR3, PIK3CA, and BRAF, which is often mutated in melanocytic nevi and melanomas.

Five (17%) of the SLs had an activating FGFR3 mutation, and 2 of 28 analyzable SLs (7%) revealed the PIK3CA/E542K hot-spot mutation commonly found in SKs. No BRAF mutations were found.

Comment: The FGFR3/PIK3CA pathway has emerged as an important target of activation in benign keratinocytic proliferations. This study provides a genetic link between SLs and SKs, raising the intriguing possibility that SL formation is driven by an interaction between keratinocytes and melanocytes rather than representing a pure melanocytic proliferation. Even more interesting is the low rate of cancer formation in SKs despite the high frequency of oncogenic FGFR3 mutations. Perhaps the real question is not why SKs and SLs form but why they so seldom lead to cancer.

— Hensin Tsao, MD, PhD

Published in Journal Watch Dermatology May 15, 2009

Citation(s):

Hafner C et al. FGFR3 and PIK3CA mutations are involved in the molecular pathogenesis of solar lentigo. Br J Dermatol 2009 Mar; 160:546.

• Medline abstract (Free)