Department of Dermatology, Venereology and Allergology, Ruhr-University Bochum, Germany.
Clin Exp Dermatol. 2012 Oct;37(7):781-5. doi: 10.1111/j.1365-2230.2012.04393.x.
Congenital unilateral linear porokeratosis (CULP) is a rare disorder of keratinization that shares clinical and molecular similarities with psoriasis. It also has an increased risk for malignant transformation to cutaneous squamous cell carcinoma (SCC). We investigated the expression of psoriasin, human beta-defensin-2, cathelicidin antimicrobial peptide/LL-37, e-cadherin, involucrin, p16(INK4a) , p53, cyclin D1 and microchromosome maintenance protein 7 in healthy skin and in lesions of psoriasis, CULP and SCC from the same patient. p16(INK4a) was overexpressed in CULP but not in the subsequent SCC. Psoriasin was overexpressed in psoriasis, CULP and SCC compared with healthy skin. Speculatively, p16(INK4a) and psoriasin could be involved in the pathogenesis of CULP. Moreover, psoriasin may play a role in the malignant transformation of CULP to SCC.
先天性单侧线性角化病（CULP）是一种罕见的角化异常疾病，其临床表现和分子特征与银屑病相似。CULP 也有向皮肤鳞状细胞癌（SCC）恶性转化的风险增加。我们研究了同一个患者的银屑病、CULP 和 SCC 皮损与健康皮肤中 psoriasin、人β-防御素-2、抗菌肽/LL-37、E-钙黏蛋白、兜甲蛋白、p16(INK4a)、p53、细胞周期蛋白 D1 和微染色体维持蛋白 7 的表达。p16(INK4a)在 CULP 中过度表达，但在随后的 SCC 中没有。与健康皮肤相比，psoriasin 在银屑病、CULP 和 SCC 中过度表达。推测 p16(INK4a)和 psoriasin 可能参与了 CULP 的发病机制。此外，psoriasin 可能在 CULP 向 SCC 的恶性转化中起作用。
