Gene expression in actinic keratoses: pharmacological modulation by imiquimod

• DOI: 10.1111/j.1365-2133.2004.06236.x
• Publication Date: 2004-12-09T21:36:30Z
• Authors: B. Lysa; U. Tartler; R. Wolf; P. Arenberger; B. Benninghoff; T. Ruzicka; U.R. Hengge; M. Walz
• Keywords: Imiquimod; TLR7; Actinic keratosis; Proinflammatory cytokine

Actinic keratoses (AKs) are premalignant lesions that can progress into squamous cell carcinoma. Imiquimod, which belongs to the new class of immune-response modifiers, was recently shown be effective in treatment AKs. The underlying mechanisms not fully understood.To study expression individual genes uninvolved skin and AKs before therapy elucidate way these is influenced by imiquimod therapy.We treated 13 patients with AK compared gene before, during (five patients) after (eight skin. We analysed coding for inflammatory cytokines or their receptors, adhesion molecules, anti-apoptotic proteins, p53 toll-like receptors (TLRs) reverse-transcriptase polymerase chain reaction.Comparing untreated AK, we found significant differences interleukin (IL)-6, hurpin, TLR7 TLR8. During therapy, detected a further upregulation interferon-alpha, IL-6, IL-10 receptor 1 TLR7. In contrast, two genes, hurpin HAX-1, were downregulated. did detect p53, tumour necrosis factor-alpha alpha- beta-catenins. Clinically, upregulated proinflammatory correlated local inflammation induced imiquimod.Our results indicate specific detectable between Imiquimod most this study. This work extends previous findings on effects regulation