p53 Protein and Proliferating Cell Nuclear Antigen Expression in Epidermal Keratinocytic Neoplasms.
- Author:
Ho Su CHUN
;
Kwang Hyun CHO
;
Chul Woo KIM
- Publication Type:Original Article
- Keywords:
Pustular Drug Eruption;
Subcorneal Pustule
- MeSH:
Actins;
Bowen's Disease;
Carcinogenesis;
Carcinoma in Situ;
Carcinoma, Squamous Cell;
Epidermis;
Keratoacanthoma;
Keratosis, Actinic;
Prognosis;
Proliferating Cell Nuclear Antigen*
- From:Korean Journal of Dermatology
1994;32(4):562-573
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Although actinic keratosis and Bowens disease ar considered as carcinoma in situ, most of them are biologically benign and dont progress to invasive squamous cell carcinoma. It is little known why they take the benign courses and which factors are involved in the tumorigenesis. Keratoacanthoma, self-regresi;ing benign tumor, may be sometimes or fused morphologically with well-differentiated squamous cell carcinoma. So it is necessary to find a useful marker to help us distinguish them. OBJECTIVES: We performed this study to gain a better understani ling of biologic behaviour and tumerigenesis of epidermal keiatinocytic neoplasms. METHODS: We investigated the expression of p53 protein and priliferating cell nuclear antigen (PCNA) by an immunohistochemical method on the formalin-fixed, araffinembedded tissue specimens of epidermal keratinocytic neoplasms. RESULTS: Fourteen out of 20 cases of squamous cell carcinoma(70.0%), 14 out of 22 cases of actinic keratosis(63.6%), and 13 out of 20 cases of Bowens disease(65.0%) showed p53 protein expression, but keratoacanthoma was negative. All the tumors studied sho ved significantly increased numbers of PCNA-positive eells when compared with normal epidermis and characteristic distribution pattern. of PCNA-positive cells. Most cases of actinic keratosis exhibited the basal dysplastic pattern, but Bo wenoid variants showed diffuse dysplastic pattern. Karatoacanthoma revealed the marginal pattern and Bowens disease showed the diffuse dysplastic pattern. Well-differentiated squamous cell carcinoria showed the basal dysplastic pattern, while poorly differentiated squamous cell carcinoma revealed d ffuse dysplastic pattern. CONCLUSION: Our results suggest that p53 mutation is a common and early genetic change in the epidermal tumorigenesis and may be used as a good marker for malignan transformation, but it does not seem to correlate with the biollagic behavior or prognosis of epidermal neoplasms. PCNA, which is considered as a proliferation-relaited marker, was expressed with chavaceristic distribution patterns according to the type of tumors, but the frequency of PCNA expression is unlikely to reflct the malignant potential of epidermal neoplasms.
