Background: Imiquimod is a modifier of the immune response that has been prov en to be an effective treatment for basal cell carcinoma (BCC). However, its mec hanism of action is still unknown. Objectives: To determin...Background: Imiquimod is a modifier of the immune response that has been prov en to be an effective treatment for basal cell carcinoma (BCC). However, its mec hanism of action is still unknown. Objectives: To determine whether imiquimod modifies the expression of proteins such as Bcl- 2, Ki67, p53 and the BCC apoptotic inde x. Patients and methods: Thirty Caucasian patients with primary BCCs larger than 8 mm in diameter were included in a double-blind randomized clinical and immu nohistochemical study which was designed in a reference university hospital. The 30 BCCs were randomized in two treatment arms between September 2001 and Februa ry 2002. Twenty-four BCCs were treated with imiquimod 5% cream and six BCCs w ith Aldara. (3M Pharmaceuticals) excipient. Histological samples were obtained b efore treatment and on days 8 and 15 during the course of treatment. The BCC exp ression of Bcl-2, Ki67 and p53 was determined in paraffin samples and the apop totic index of the BCC was studied using the TUNEL technique (terminal deoxynucl eotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labelli ng) in frozen samples. All variables were evaluated quantitatively in fields wit h a magnification× 400. Results: The BCCs treated with imiquimod showed a decre ase in the expression of Bcl-2 (88- 7% before treatment, 61.4% day 15, P = 0.01) and an increase in the apoptotic index (0.53% before treatment, 1.66% day 15, P = 0- 002), which were not observed in the BCCs treated with the exc ipient. Ki67 and p53 did not show significant changes in any group. Conclusions: Imiquimod reduces the expression of Bcl- 2 in the BCC cells and increases the BCC apoptotic index.展开更多
文摘Background: Imiquimod is a modifier of the immune response that has been prov en to be an effective treatment for basal cell carcinoma (BCC). However, its mec hanism of action is still unknown. Objectives: To determine whether imiquimod modifies the expression of proteins such as Bcl- 2, Ki67, p53 and the BCC apoptotic inde x. Patients and methods: Thirty Caucasian patients with primary BCCs larger than 8 mm in diameter were included in a double-blind randomized clinical and immu nohistochemical study which was designed in a reference university hospital. The 30 BCCs were randomized in two treatment arms between September 2001 and Februa ry 2002. Twenty-four BCCs were treated with imiquimod 5% cream and six BCCs w ith Aldara. (3M Pharmaceuticals) excipient. Histological samples were obtained b efore treatment and on days 8 and 15 during the course of treatment. The BCC exp ression of Bcl-2, Ki67 and p53 was determined in paraffin samples and the apop totic index of the BCC was studied using the TUNEL technique (terminal deoxynucl eotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labelli ng) in frozen samples. All variables were evaluated quantitatively in fields wit h a magnification× 400. Results: The BCCs treated with imiquimod showed a decre ase in the expression of Bcl-2 (88- 7% before treatment, 61.4% day 15, P = 0.01) and an increase in the apoptotic index (0.53% before treatment, 1.66% day 15, P = 0- 002), which were not observed in the BCCs treated with the exc ipient. Ki67 and p53 did not show significant changes in any group. Conclusions: Imiquimod reduces the expression of Bcl- 2 in the BCC cells and increases the BCC apoptotic index.
