Immunohistochemical expression of P53, Ki-67, and CD34 in psoriasis and psoriasiform dermatitis

Abstract

Background: Psoriasis is the prime example of psoriasiform tissue pattern and should be differentiated from other psoriasiform dermatoses both clinically and histopathologically.Aim: To evaluate immunohistochemical expression of P53, Ki-67, and CD34 in psoriasis and psoriasiform dermatitis for diagnostic purposes.Methods: An analytical cross-sectional study was performed on the paraffin blocks of 60 psoriasis and 31 psoriasiform dermatitis patients between 2014 and 2017. The selected formalin-fixed paraffin-embedded tissues from each biopsy specimen were cut into 4-micron sections. Initial sections were stained by hematoxylin and eosin staining. Primary antihuman antibodies against P53, Ki-67, and CD34 were applied. Positive control samples for biomarkers were received from former strongly positive samples of papillary endothelial hyperplasia, high grade lymphoma, and breast ductal carcinoma for CD34, Ki-67, and P53, respectively.Results: Out of 60 psoriasis patients, 56.7% were men, with the mean age of 36.8 years. From 31 psoriasiform patients, 45.2% were men, with the mean age of 37.5 years. Both groups were matched in terms of sex and age. The mean staining of three markers was more significant in psoriasiform dermatitis than psoriasis.Conclusion: In spite of some other researches, the present study showed expression of P53, Ki-67, and CD34 biomarkers were significantly higher in psoriasiform dermatitis than psoriasis.

Advanced Characterization of Imiquimod-Induced Psoriasis-Like Mouse Model

“…On the other hand, hyperproliferation can be revealed through the observation of proliferative markers such as Ki-67 and the proliferating cell nuclear antigen (PCNA). The increase of these nuclear proteins in psoriasis has already been shown in literature [23,44].…”

“…In addition, PECAM/CD31 plays a role in angiogenesis, platelet aggregation, homeostasis, and in the maintenance of vascular endothelial barrier function [19]. As a second marker, the presence of CD34 positive endothelial cells has been observed in psoriasis since this transmembrane protein is involved in the adhesion phenomenon of blood vessels [20][21][22][23]. Thus, we used both anti-CD31 and anti-CD34 staining to confirm the usefulness of these parameters in the IMQ mouse model for the study of angiogenesis and dermal vascularity changes.…”

Comparison of p53 immunohistochemical staining in differentiated vulvar intraepithelial neoplasia (dVIN) with that in inflammatory dermatoses and benign squamous lesions in the vulva

“…Our cases of PSO and CAN showed patchy weak to moderate p53 staining in both the basal cells and the parabasal cells. In the literature, p53 staining in non‐vulvar PSO has been shown to be variable, ranging from negative to patchy positivity to overexpression as compared with normal or non‐lesional skin 34 ; however, the staining patterns were not clearly defined. TP53 mutations have not been shown to be implicated in PSO, and the increased p53 expression is thought to be due to a physiological response to increased epidermal proliferation 35 .…”

“…The staining in LS and squamous hyperplasia was seen in <10% of the basal cells, and none showed suprabasilar extension 8 . Knowledge of the staining characteristics of p53 in other benign squamous lesions is sparse, and the limited studies available lack sufficient detail, only reporting the overall proportion of cells stained, without detailing the distribution (basal or suprabasal), intensity or consistency (uniform or heterogeneous) of staining 29–38 …”

“…8 Knowledge of the staining characteristics of p53 in other benign squamous lesions is sparse, and the limited studies available lack sufficient detail, only reporting the overall proportion of cells stained, without detailing the distribution (basal or suprabasal), intensity or consistency (uniform or heterogeneous) of staining. [29][30][31][32][33][34][35][36][37][38] In this study, we examined p53 immunostaining patterns in dVIN, and in vulvar inflammatory lesions in its differential diagnoses, to determine whether p53 can be used to distinguish dVIN from benign mimics in the vulva.…”