Expression of p16 in Hypertrophic Lichen Planus

Although cutaneous squamous cell carcinoma (SCC) arising from lichen planus is rare, hypertrophic lichen planus (HLP) accounts for most of these malignant transformations. Although the mechanism of malignant pathogenesis remains unknown, reports of similar premalignant conditions suggest a potential role of tumor suppressor p16. This is the first study to our knowledge to examine p16 expression in HLP in comparison to cutaneous invasive SCC and normal skin and its implications for malignant transformation.

p16 immunohistochemistry of HLP (n = 34) was performed alongside location-matched well-differentiated SCC (WDSCC) and normal skin. Percentage of positive cells, nuclear and cytoplasmic staining intensity, and staining distribution patterns were reviewed by 2 Board-certified dermatopathologists.

HLP and WDSCC both showed an increased percentage of positive cells compared with normal skin ( P < 0.001). Cytoplasmic p16 was overexpressed in HLP compared with WDSCC ( P < 0.05). Most cases of HLP and WDSCC demonstrated stronger basal and suprabasal keratinocyte staining with weaker superficial staining. In WDSCC, a predominant pattern of focal cytoplasmic margination of staining along the cellular periphery was observed.

Our finding of cytoplasmic p16 overexpression in HLP suggests a potential mechanism of p16-mediated cell cycle dysregulation seen in other premalignant conditions. p16 overexpression seems to be a possible contributor in the malignant transformation of HLP to SCC.