Nelson C, Cowper S, Morgan M
Department of Pathology, University of South Florida College of Medicine, Tampa, USA.
Am J Dermatopathol. 1999 Oct;21(5):420-5. doi: 10.1097/00000372-199910000-00003.
The etiology of the porokeratoses is unknown. Overexpression of the p53 tumor suppressor protein and disregulated cell cycle control have been pathogenically implicated. The p53 tumor suppressor gene product is regulated by mdm2 and both gene products influence cell cycle progression through the cyclin-dependent kinase inhibitor p21. Thirty-three cases of the various types of porokeratosis were immunohistochemically studied for p53, mdm2, and p21 proteins. Each of the cases showed increased p53 and decreased mdm2 and p21 expression within keratinocytes underlying cornoid lamella. This study confirms the previous findings of increased p53 staining and expands the potential roles of mdm2 and p21 in the pathogenesis of the porokeratoses.
汗孔角化症的病因尚不清楚。p53肿瘤抑制蛋白的过度表达和细胞周期调控失调在发病机制上与之相关。p53肿瘤抑制基因产物受mdm2调控，且这两种基因产物均通过细胞周期蛋白依赖性激酶抑制剂p21影响细胞周期进程。对33例不同类型的汗孔角化症进行了p53、mdm2和p21蛋白的免疫组织化学研究。每例病例在鸡眼样板下方的角质形成细胞中均显示p53表达增加，mdm2和p21表达降低。本研究证实了先前p53染色增加的发现，并扩展了mdm2和p21在汗孔角化症发病机制中的潜在作用。
