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.
From the Department of Pathology (S.C., M.M.), University of South Florida College of Medicine, and the Department of Dermatopathology (M.M.), Haley Veteran's Administration Hospital, Tampa, Florida. Mr. Nelson is a second-year medical student at the University of Missouri-Kansas City.
This paper reflects the opinions of solely the authors. It does not reflect the opinions of the Department of Veteran's Affairs or of the United States Government.
Address correspondence to Michael Morgan, M.D., Department of Dermatopathology, James A. Haley Veterans' Hospital, 13000 Bruce B. Downs Blvd., Tampa, FL 33612.