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Systemic treatment with retinoids is promising in chemoprevention of actinic keratosis and squamous cell carcinoma in renal transplant recipients (RTRs).¹ It is currently unknown how retinoids exert their chemopreventive effect. Recently, we demonstrated that retinoids alter differentiation in warts of RTRs, with induction of keratin 13 (K13) expression in a specific zebroid pattern.² In view of the clinical efficiency of retinoids, it is feasible that they not only influence keratinization but also interfere with the expression of cell cycle–associated proteins like the proliferation marker MIB-1, and the tumor suppressors p53 and p16^INK4A. Recent data revealed that both the p53 pathway and the p16^INK4A pathway are involved in cutaneous carcinogenesis.³ The effects of retinoid treatment on expression of cell cycle–associated proteins in premalignant epidermal lesions of RTRs are unknown.

In this prospective immunohistochemical study, the effects of 3 months' withdrawal of long-term acitretin treatment on the expression of K13, MIB-1, . . . [Full Text of this Article]

Methods


Results
K13

MIB-1, p16^INK4A, and p53

Comment