Track

Clinical Studies

Abstract

Benign vascular proliferations, including various types of hemangiomas and non-hemangiomatous proliferations, constitute a diverse diagnostic category observed across different patient populations, each with varied pathogenesis and clinical courses. The unifying feature of these lesions is the proliferation of endothelial cells lining vascular channels. Other histological features may also accompany these proliferations, such as epidermal hyperplasia seen in angiokeratomas. P16 is a useful marker for detecting a tumor suppressor gene encoded by CDKN2A, which prevents the cell cycle from progressing into the S phase. Its expression is known to increase aging cells, promoting apoptosis. P16 expression was evaluated in infantile hemangioma and was found to exhibit different expression levels in different phases of lesional evolution. This variation in expression may suggest that p16 plays an important role in angiogenesis. While this relationship has only been observed only in infantile hemangiomas and has not been conducted in other vascular lesions, we aimed to test p16 in relation to various benign vascular proliferations and different proliferation stages of other entities as well. We assessed P16 expression in 18 different benign vascular proliferations, such as infantile hemangioma, capillary hemangioma, hobnail hemangioma, pyogenic granuloma, angiokeratoma, and spindle cell hemangioma. Our findings show different patterns of expression in different types of proliferations, indicative of varying pathogenesis and clinical features. If this relationship proves predictive of the clinical course, p16 could potentially serve as a marker for identifying which lesions may spontaneously regress or provide a pathway for non-disfiguring therapies and possibly potential gene therapies.