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. 2023 Nov 24;12(23):7291.
doi: 10.3390/jcm12237291.

Expression of p53, p63, p16, Ki67, Cyclin D, Bcl-2, and CD31 Markers in Actinic Keratosis, In Situ Squamous Cell Carcinoma and Normal Sun-Exposed Skin of Elderly Patients

Alise Balcere  1 , Māris Sperga  2 , Ingrīda Čēma  3 , Gunārs Lauskis  3 , Maksims Zolovs  4   5 , Māra Rone Kupfere  1 , Angelika Krūmiņa  6
Affiliations

Expression of p53, p63, p16, Ki67, Cyclin D, Bcl-2, and CD31 Markers in Actinic Keratosis, In Situ Squamous Cell Carcinoma and Normal Sun-Exposed Skin of Elderly Patients

Alise Balcere et al. J Clin Med. .

Abstract

Background: Age and cumulative exposure to ultraviolet (UV) light are primary contributors to skin cancer development. Regulatory proteins within the cell cycle are essential for the homeostasis of squamous epithelium.

Methods: This study assessed the expression of immunohistochemical markers p53, p63, p16, Ki67, Cyclin D, Bcl-2, and CD31 in keratinocyte intraepithelial neoplasia (actinic keratosis and squamous cell carcinoma in situ) compared to normal skin. The objective was to distinguish disease-specific changes from those attributable to ageing and sun exposure in elderly skin.

Results: Analysis included 22 actinic keratoses (AK), 7 in situ squamous cell carcinomas (SCC), and 8 normal skin biopsies. The mean age was 78.1 years for the AK/SCC group and 73.8 years for controls, with no significant age difference noted between the groups. The AK/SCC group exhibited a higher occurrence of amorphous masses, higher intensity of p53, lower Bcl-2 expression in the epidermis, higher Bcl-2 expression in the dermis, and higher CD31 expression in the dermis, all of which were statistically significant (p < 0.05).

Conclusions: The study identifies distinct differences in the presence of amorphous masses and the expression levels of p53, Bcl-2, and CD31 between sun-exposed skin and in situ cutaneous squamous cell carcinomas, including actinic keratoses.

Keywords: UV damage; age; cell cycle regulatory markers; immunohistochemistry; skin cancer.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Immunohistochemical expression of p53, p63, p16, and Cyclin D in actinic keratosis (A–D) and control (E–H) skin. Black arrows indicate strong positive cell staining. (A) expression of p53 in actinic keratosis (AK) with weak staining if any; (B) expression of p63 in AK, distribution above 2/3 of epidermal thickness; (C) expression of p16 in AK with 1–30% nuclear staining; (D) expression of Cyclin D in AK, distribution up to 2/3 of epidermal thickness; (E) expression of p53 in control skin (CS) with <5% nuclear staining; (F) expression of p63 in CS, distribution above 2/3 of epidermal thickness; (G) expression of p16 in CS with <1% nuclear staining; (H) expression of Cyclin D in CS, distribution up to 2/3 of epidermal thickness.
Figure 2
Figure 2
Immunohistochemical expression of Ki67, Bcl-2, and CD31 in actinic keratosis (A–C) and control (D–F) skin; (A) expression of Ki67 in actinic keratosis (AK), distribution up to 2/3 of epidermal thickness; (B) expression of Bcl-2 in AK, distribution up to 2/3 of epidermal thickness, foci with pronounced subepidermal infiltration (red arrows); (C) expression of CD31 in AK, visible pronounced expression; (D) expression of Ki67 in control skin (CS), distribution of up to 1/3 of epidermal thickness; (E) expression of Bcl-2 in CS, distribution up to 2/3 of epidermal thickness, weak or none subepidermal infiltration; (F) expression of CD31 in CS, few visible positive capillaries. Black arrows indicate positive cell staining in the epidermis (A,B,D,E) and positive endothelial staining (C,F).
See this image and copyright information in PMC

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