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Norbert M. Wikonkal, MD; Rob J. W. Berg, PhD; Christian W. van Haselen, MD; Irene Horkay, MD, PhD; Eva Remenyik, MD; Agnes Begany, MD; Janos Hunyadi, MD, PhD; Willem A. van Vloten, MD; Frank R. de Gruijl, PhD

Arch Dermatol. 1997;133(5):599-602.

Abstract
Background
A failure in the apoptotic response after severe genomic damage could facilitate cell transformation and tumor development, and a constitutive overexpression of either p53 or bcl-2 protein in nonapoptotic tumor cells could signify a defective bax-mediated apoptosis. Objectives: To investigate whether a negative correlation occurs between these 2 proteins in nonmelanoma skin cancer and whether overexpression of either protein is associated with a low rate of spontaneous apoptosis. Design: Immunohistochemical study of nonmelanoma skin cancer archive material.

Setting
University referral center. Patients: White patients with tumors on sun-exposed skin areas (ie, 17 basal cell carcinomas and 22 squamous cell carcinomas).

Main Outcome Measures
Positivity for p53 and bcl-2 were scored semiquantitatively on 4 levels, and the percentages of apoptotic cells were determined.

Results
A significant negative correlation between p53 and bcl-2 expression was found in the basal cell carcinomas, but not in the squamous cell carcinomas, largely attributable to the low level of bcl-2 staining in the squamous cell carcinomas. Squamous cell carcinomas have a significantly higher number of apoptotic cells than basal cell carcinomas: 1.1% vs 0.6%, respectively. This spontaneous apoptosis decreases with increasing bcl-2 (in basal cell carcinoma), whereas it does not appear to be related to p53 level expression.

Conclusions
These results indicate that a disturbance in either p53 or bcl-2 suffices to enhance skin tumor formation by suppressing apoptosis; bcl-2 appears to reduce the rate of spontaneous apoptosis, but an aberrant p53 expression does not, and this factor may solely affect the apoptosis from exogenous genotoxicity.

Arch Dermatol. 1997;133:599-602

Author Affiliations
From the Departments of Dermatology, University of Utrecht, Utrecht, the Netherlands (Drs Wikonkal, Berg, van Haselen, van Vloten, and de Gruijl), and University Medical School of Debrecen, Debrecen, Hungary (Drs Wikonkal, Horkay, Remenyik, Begany, and Hunyadi).

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