Malignant melanoma arising from nevi, p53, p16, and Bcl-2: expression in benign versus malignant components.
BACKGROUND
The etiology of malignant melanoma has been the subject of much study. Tumour suppressor genes p53 and p16 and the antiapoptotic, Bcl-2, are implicated in the development and progression of malignant melanoma.


OBJECTIVE
To compare the expression of p53, p16, and the Bcl-2 genes in both benign and malignant components of malignant melanoma arising from pre-existing nevocellular nevi.


METHODS
Twenty cases of malignant melanoma arising from pre-existing nevi were selected and studied by immunohistochemistry for the expression of p53 (D07) CDK4I/MTS-1/INK <4, which detects both wild and mutant type, p16 CDK4I/MTS-1/INK <4, and Bcl-2 using an avidin-biotin technique on formalin-fixed, paraffin-embedded sections.


RESULTS
Fifteen cases demonstrated p53 immunoreactivity in the malignant components ranging from 5 to 20% with no expression being seen in the benign components. The p16 gene showed strong nuclear reactivity in the benign components of 14 cases and weak reaction in 6 cases; the malignant components expressed weak nuclear staining in 18 cases and cytoplasmic staining in all cases. The Bcl-2 gene was expressed strongly to moderately in benign components and weakly in malignant components of nine cases, and was negative in 11 cases.


CONCLUSIONS
Immunostaining for p53 is expressed only in the malignant component, whereas p16 and Bcl-2 showed decreased staining and a different pattern in malignant compared with benign components. These findings suggest that expression and alterations in the subcellular localization of the cell cycle regulators may contribute to the mechanism of tumourigenesis.
Radhi
J M
JM
Department of Pathology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
D002471:Cell Transformation, Neoplastic; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D008545:Melanoma / Q000235:genetics / Q000473:pathology*; D009506:Nevus / Q000235:genetics / Q000473:pathology*