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Journal of Skin CancerVolume 2011 (2011), Article ID 571734, 6 pagesdoi:10.1155/2011/571734 © 2011 Mary H. Lien and Vernon K. Sondak.

The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]

Clinical clearance rate at 1, 2 and 3 years were 94, 76 and 70%, respectively. We conclude that imiquimod seems to be an appropriate therapeutic alternative for the treatment of recurrent BCC in patients with associated co-morbidities.

Clinical clearance rate at 1 and 2 years were 89% and 85%, respectively.