Abstract
Treatment with imiquimod 5% cream, capable of inducing interferon (IFN)-alpha, effectively cures basal cell carcinoma (BCC), both clinically and histologically. IFN-alpha induces expression of CD95-receptor (FasR) on BCC cells, which normally fail to express Fas receptor (FasR). Expression of the FasR is postulated to lead to apoptosis via CD95 receptor-CD95 ligand (FasL) interaction. Absence of this receptor may be responsible for the longevity of the cells of BCCs by preventing them undergoing 'suicidal' apoptosis, as well as apoptosis induced by neighbouring BCC cells and/or by infiltrating T-lymphocytes. We examined the expression of FasR on BCC after very short-term exposure to imiquimod 5% cream or vehicle. In a double-blind study, 10 patients with BCC applied either imiquimod (n = 5) or vehicle (n = 5) five times per week for up to 2 weeks. At the end of treatment, the treated area was excised and examined for the presence or absence of FasR by immunoperoxidase staining of rat antihuman FasR with haematoxylin and eosin counterstaining. Histologically, BCC cells were present in all (5/5) of the vehicle-treated BCCs and in 4/5 of the imiquimod-treated BCCs. BCC cells expressed FasR in 3/4 imiquimod-treated BCCs but in none (0/5) of the vehicle-treated tumours. T-lymphocytes apposed to BCC cells were evident in all three imiquimod-treated BCCs expressing FasR and in none of the FasR-negative, vehicle-treated BCCs. Imiquimod-induced FasR-mediated apoptosis may contribute to the effectiveness of imiquimod 5% cream for the treatment of BCC.
