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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]

This article discusses new Duke University research showing a highly significant correlation (p = 0.007) between higher vitamin D intake and MRI brain lesions (http://www.fasebj.org/cgi/content/meeting_abstract/21/6/A1072), as well as the potential for lesion reversal. These lesions have been associated with cognitive impairment, stroke, psychiatric disorders and mortality. This article also discusses the levels of vitamin D and calcium needed to avoid osteoporosis and vascular calcification in the light of new research on blockage of the vitamin D receptor due to bacterial products and elevated 25D.

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

"new research demonstrates that ingested vitamin D is immunosuppressive and that low blood levels of vitamin D may be actually a result of the disease process. Supplementation may make the disease worse. "

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