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Claudin‐1 expression decreases with increasing pathological grade in actinic keratosis and may be a marker of high‐risk actinic keratosis
Author(s) -
Lee J. S.,
Park H. S.,
Yoon H. S.,
Cho S.
Publication year - 2019
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.13810
Subject(s) - actinic keratosis , pathological , pathogenesis , medicine , dysplasia , dermatology , langerin , immunohistochemistry , seborrheic keratosis , pathology , basal cell , immunology , dendritic cell , immune system
Summary Background Actinic keratosis ( AK ) is a common sun‐induced skin disorder that can progress to invasive squamous cell carcinoma. However, there is still no reliable method to predict high‐risk AK . Aim To identify markers that reflect the biological behaviour of AK and to understand the pathogenesis of AK . Methods In total, 52 patients with AK and 17 site‐matched healthy controls ( HC s) were enrolled. We evaluated solar elastosis and immunohistochemical features using antibodies to p53, vitamin D receptor ( VDR ), claudin‐1 and Langerin ( CD 207). Comparisons between AK and HC skin were performed and analyses carried out according to the pathological grade of AK . Results We found that in both patients and HC s, solar elastosis increased and Langerhans cell ( LC ) density decreased with ageing. Solar elastosis and p53 expression were higher and VDR expression was lower in patients than in HC s; however, there was no statistical difference between them in relation to the pathological grade of AK . Claudin‐1 expression gradually decreased from HC skin to severe AK , and particularly decreased in areas with epidermal atypia. LC density in severe AK was significantly lower than in HC skin and mild AK , while there was no difference in LC density between HC skin, mild AK and moderate AK . Conclusions Claudin‐1 could be a useful marker of the pathological severity of AK . In addition, p53 increases and VDR decreases in AK , not in a gradual manner but in the early steps of carcinogenesis. LC density is relatively maintained in AK until it reaches severe dysplasia.