Immunohistochemical Expression of p16 and p21 in Melanocytic Nevi and Malignant Melanoma.
- Author:
Jung Woo SUN
1
;
Byoung Soo CHUNG
Author Information
1. Department of Dermatology, Chosun University Medical School, Kwangju, Korea.
- Publication Type:Original Article
- Keywords:
p16;
p21;
Melanocytic nevi;
Malignant melanoma
- MeSH:
Antibodies, Monoclonal;
Carcinogenesis;
Cell Cycle;
Cell Proliferation;
Cyclins;
Dermis;
Humans;
Life Cycle Stages;
Melanoma*;
Nevus;
Nevus, Intradermal;
Nevus, Pigmented*;
Phosphotransferases;
Prognosis
- From:Korean Journal of Dermatology
2000;38(11):1492-1498
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: p16 and p21 belong to the family of cyclin dependent kinase inhibitors, which are important negative regulators of the cell cycle. Loss of normal cell cycle regulation contributes to the development and progression of malignancies. Typical acquired melanocytic nevi appear to follow a life cycle characterized by active growth, maturation, and progressive involution. In contrast, congenital melanocytic nevi have a different course and prognosis with potential for development of melanoma, and metastatic spread is very common in malignant melanoma. OBJECTIVE: We investigated the expression patterns of p16 and p21 in acquired and congenital melanocytic nevi, and malignant melanoma by immunohistochemical technique. METHOD: Formalin-fixed and paraffin-embeded tissue from 3 junctional nevi, 5 compound nevi, 7 intradermal nevi, 5 congenital melanocytic nevi, and 5 malignant melanoma were immunolabeled with monoclonal antibodies directed against p16 and p21. RESULT: The benign melanocytic nevi showed a high expression for p16, and the expression of p21 was low or undetectable in benign melanocytic nevi with the exception of positive staining in junctional nevus, involuting intradermal nevus, and nevus cells in deep dermis of congenital meanocytic nevi. In malignant melanoma, the expression of p21 was higher than p16 expression with variable intensity of staining in different areas of the tumor. These findings suggest that the loss of p16 and expression of p21 seem to be related to tumorigenesis of melanocytic tumors. The expression of p21 which is induced by feedback mechanism in attempt to halt increased cell proliferation, might not be enough to restrict tumor progression and may be involved in the regressive changes of the intradermal nevi.
