Bailey et al. of UV strength (we.e. 10 a.m.-4:00 p.m.) also to make use of protecting hats and clothes prevent artificial UV radiation sources (e.g. tanning beds) and regularly apply sunscreens. It is important to note that the efficacy of sunscreens is determined by their ability to protect against UV-induced sunburns and the SPF number on sunscreen labels represents its “sunburn protection factor.” The value of sunscreens for protecting humans against NMSCs melanoma photo-aging and UV-induced immune-suppression remains MAT1 largely undetermined. Although sunscreens may play an important role in preventing skin cancer it should be noted that they also have a number of limitations. There is inconsistent compliance in the use of most sunscreens because they are greasy and messy and stain clothing. Although large amounts of sunscreen are generally required to achieve the full SPF value displayed on the label most people apply only about 25% of this amount (6). Furthermore UVB radiation is required for the cutaneous photoconversion BINA of 7-dehydrocholesterol to previtamin D and sunscreens may limit this conversion (7). Potential effects of sunscreens on vitamin D metabolism may not concern most people but they may be an issue for the elderly and other people with vitamin D deficiency. Last sunscreens have no effect on prior UV-mediated skin tissue damage. The few reported studies of sunscreen effects suggest that sunscreens reduce the incidence of SCCs and actinic keratoses but are much less effective in preventing BCCs (8-11). Regular application of sunscreen for seven months significantly reduced the ratio of new actinic keratoses to total actinic keratoses (versus vehicle) in individuals with prior actinic damage (8). Another controlled trial found that people who applied sunscreen regularly for five years had a statistically significant 35% lower incidence of cutaneous SCCs but not a statistically significantly lower incidence of BCCs (compared with placebo) BINA (9 10 A more recent controlled trial lasting 24 months in 120 heart lung and kidney transplant recipients showed a significant reduction in actinic keratoses and SCCs in people who used a highly protective sunscreen regularly compared with individuals who did not. BCCs also declined in the sunscreen group but not statistically significantly (12). Researchers have shown great interest in identifying new ways other than sunscreen to prevent UV-induced NMSCs. Oral retinoids (13 14 and topical DNA repair enzymes are chemopreventive methods with reported effectiveness in human beings (15). Both techniques were effective primarily in patients having a predisposition to build up pores and skin tumor including xeroderma pigmentosum individuals who’ve a hereditary defect in the repair of UV-damaged DNA and immunosuppressed organ-transplant recipients. Low-fat diets also have reduced the incidence of NMSCs but compliance with low-fat diets is not so easily achieved (16). Research into the pathogenesis of BCC and SCC has stimulated interest in chemopreventive agents that inhibit the activity of cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC) both of which contribute to UVB-induced skin cancer development. In murine models as well as in humans UVB BINA enhances the expression of COX-2-dependent prostaglandin (PG) production particularly of PGE2 BINA (17-20). COX-2 and PGE2 have important roles in skin carcinogenesis (18) stimulating the proliferation of preneoplastic cells and promoting inflammation during the promotion stage. They also facilitate the epithelial-to-mesenchymal transition suppress host anti-tumor defense mechanisms inhibit tumor-cell apoptosis and stimulate angiogenesis during the progression stage of skin BINA carcinogenesis. Not expressed in undamaged normal epidermis COX-2 can be induced in such tissue by severe and chronic contact with UVB (18) and it is overexpressed in the epithelia of actinic keratoses and SCCs (20). COX-2 BINA can be within BCC where its distribution differs from that of SCCs. COX-2 is situated in the stroma encircling islands of epithelial BCC cells in mice and mainly in the cells next to BCC islands in human beings (20). Treating.