Enhanced Expression of p53 Protein in Pityriasis Rubra Pilaris

Abstract

p53 is a phosphoprotein, known since 1992 as a “guardian” of the genome (1, 2). A mutation in the p53 gene coding this protein, which activation protects the organism from tumourigenesis, has been found in more than half of all human tumour types (3). DNA damaging agents induce p53 protein activity, which leads to cell cycle arrest in the G1 or G2 phase and, in the case of ineffective DNA repair, apoptosis is initiated (4). p53 immunoreactivity has also been found in non-tumourigenic inflammatory skin diseases, e.g. psoriasis, chronic dermatitis, lupus erythematosus and lichen planus (5), often with contro-versial results. p53 is also detectable in normal skin, using various methods of antigen retrievals, especially after ultraviolet (UV) exposure, but at very low levels (6).Pityriasis rubra pilaris (PRP) is a rare hyperkeratotic, papulo-squamous skin disorder with unknown aetio-logy. Although the first case was described in 1828, until now the pathogenesis of this rare disorder is still a matter for debate. A few possible mechanisms are considered: abnormal vitamin A metabolism in the skin, association with internal malignancies, immune system dysregulation (PRP often appears simultaneously with autoimmune diseases) and associations with infections, particularly human immunodeficiency virus. Hereditary forms of PRP are very rare (7, 8). Experimental stu-dies showed that epidermal cells in PRP lesions have increased labelling index compared with normal skin keratinocytes, similarly to findings in psoriatic skin (9, 10). PRP presents with some histological features simi-lar to psoriasis, especially hyperkeratosis, parakeratosis and acanthosis (7, 8, 11), which could result from cell cycle disturbances in the keratinocytes.The present study was undertaken to evaluate ex-pression of p53 protein in the lesional skin of patients with type I classic PRP (confirmed by histological examination).PATIENTS AND METHODS