Korean J Dermatol.
1999 Sep;37(9):1286-1295.
Expression of p53, pRb, p16, p21 and PCNA on Psoriatic Epidermis
- Affiliations
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- 1Department of Dermatology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
Abstract
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BACKGROUND: Psoriasis is a chronic disorder which is characterized by hyperproliferation and abnormal differentiation of keratinocytes with T-cell infiltration. There is increasing evidence that inactivation of tumor-suppressor genes can promote uncontrolled cell proliferation and tumor formation. The products of p53, Rb, p16, p21 genes are examples of the molecules regulating the cell growth cycle.
OBJECTIVE
In this study, immunohistochemical analysis of cell cycle-related molecules (p53, pRb, p16, p21Waf1, and PCNA) was done to elucidate the roles and interactions of those molecules in the pathogenesis of psoriatic keratinocytes.
MATERIALS AND METHODS
Formalin-fixed skin samples composed of 20 chronic plaque type psoriatic, 20 nonlesional and 20 normal epidermis, and 5 squamous cell carcinomas were included in this study.
RESULTS
Our results suggest that p53 protein accumulation is an early event in cutaneous SCC, but not in psoriasis. In our study, diffuse expression of p16 with almost negative expression of pRb in psoriatic epidermis suggest that inverse relationship is maintained. Although loss of p16 expression is frequently associated with many kinds of cancers, we speculate there is a possibility that is a strong expression of p16 is related to localized cancer as well as in benign hyperproliferative lesions. In psoriasis, p21 may be overexpressed via a p53-independent pathway. The number of PCNA positive cells was higher in the psoriatic epidermis in contrast to scattered staining in the psoriatic nonlesional and normal epidermis
CONCLUSION
The proliferative status of psoriatic keratinocytes dose not implicate Rb gene and may not implicate the p53 gene significantly. It is associated with the strong expression of PCNA and moderately increased expressions of p16 and p21.