**1. Introduction**

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210 Highlights in Skin Cancer

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Ultraviolet radiation (UVR) has been identified as the primary etiologic agent for the induction and promotion of most skin cancers. The first associations between solar UVR and skin cancer were acknowledged by the scientific community in 1927. Since then, increasing evidence for the role of UVR in the causation of skin cancer has resulted in the listing of solar and artificial UVR as a human carcinogen by the International Agency for Research on Cancer (IARC) in 1992. Broad spectrum (UVA and UVB) UVR was categorized as a human carcinogen by the National Toxicology Program in 2005. UVR from the sun causes approximately 90% of malignant melanomas and non-melanoma (basal cell carcinoma [BCC] and squamous cell carcinoma [SCC]) skin cancers [1]. The non-melanoma skin cancers make up one third of all cancers around the world [2]. According to the National Cancer Institute, in the United States melanoma has one of the fastest increasing incidence rates. It is estimated that more than two million new cases of skin cancer will be diagnosed in 2012 [3-5]. Prevention of skin cancer is possible since UVR is known to be the central causative agent. National educational programs have emerged globally to deliver the message that unprotected sun exposure increases the risk for developing skin cancer, and present multiple behaviors that when followed together reduce the risk of photocarcinogenesis.

The goal of this chapter is to present a variety of skin cancer prevention strategies in the context of existing scientific knowledge on photocarcinogenesis. The connection between UVR exposure and skin cancer has been shown in numerous epidemiological, *in-vivo*, and *in-vitro* studies. Health professionals and government agencies have been communicating the dangers of UV exposure and the benefits of adopting primary and secondary prevention practices to lessen skin cancer incidence and mortality [1, 6]. Primary prevention strategies to protect against skin cancer are to wear broad spectrum sunscreen, seek shade, avoid the outdoors during peak daytime hours, and to wear protective clothing. Intentional UVR exposure for the purpose of tanning (indoor or outdoor) or stimulation of vitamin D synthesis is strongly

© 2013 Passantino et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

discouraged. There is scientific evidence that indicates oral and topical supplementation with antioxidants, vitamins, and phytochemicals is beneficial for chemoprevention. Secondary prevention for skin cancer is performing periodic examinations of the skin for suspicious growths, and having dangerous-looking growths excised by a dermatologist. Practicing a combination of these skin cancer prevention strategies will reduce the risk of skin cancer.

damage could carry mutations if the repair was not carried out perfectly [18]. There is a greater tendency for damaged keratinocytes to undergo apoptosis than damaged melanocytes, possibly to preserve melanin-producing cells for photoprotection [19]. In addition to genotoxic effects, UVB exposure increases cell proliferation as is observed in animal models where hyperproliferation of the epidermis and inflammation are the result of prostaglandin and

Skin Cancer Prevention Strategies http://dx.doi.org/10.5772/55241 213

UV exposure causes immunosuppression that promotes the development of skin cancer because the immune system is less likely to detect and eliminate cancer cells. UVA and UVB separately can suppress cutaneous immune responses in humans, and the magnitude of immunosuppression is greater when they are combined [20]. UVR induces physical alterations to cell surface proteins in the epidermis. These structural changes create neoantigens that would be attacked by the immune system. It is believed that the human adaptive immune system has evolved such that recognition of antigens is suppressed by UVR, thus reducing the risk of auto-sensitization. Langerhans cells, the antigen presenting cells of the skin, migrate out of the epidermis to local lymph nodes for several days after UV exposure [18]. The Langerhans cells activate T helper type 2 cells, which suppress immune reactions by releasing immunosuppressive cytokines [13, 21]. The downside to this mechanism is that cancer

UVR is considered to be a complete carcinogen since it can induce tumor formation by itself, and both UVA and UVB contribute to skin carcinogenesis. Since UVB is a more potent and direct inducer of DNA damage than UVA, it is thought to play more of a role in the initiation stage of tumorigenesis while the effects of UVA are thought to promote the development of the tumor [7]. UVR can be coupled with other chemical carcinogens to promote tumor development. The combination of solar UV and sodium arsenite causes SCC in mice, but sodium arsenite alone cannot cause SCC. This is an example of how UVR can

detection capabilities are suppressed in addition to autoimmune reactions [18].

**3. Susceptibility factors for UV-induced skin damage and cancer**

Relative endogenous protection capacity against UVR is a major factor in determining susceptibility to skin cancer. Individual differences in skin pigmentation, DNA repair, endogenous antioxidant levels, and impact the biological response to UVR [17]. The Fitzpatrick skin type (FST) was created in the 1970s as a method to classify people by the intensity of their erythema response to UVR. It can be used to predict response and susceptibility to skin cancer since lighter-skinned individuals with low FST tend to be more sensitive to UVR than darkerskinned individuals with high FST. There are six FSTs, with FST I being the most sensitive to sunlight and FST VI being the least sensitive. People that are FST I have white skin, may have freckles, blue or green-colored eyes, and red hair. People that are FST VI have black skin and hair, dark-brown eyes, and rarely experience sunburn [8]. Constitutive skin color should not be confused with FST because FST is based on the biological response not ethnicity [23]. It is no coincidence that the highest incidence rates of non-melanoma skin cancer are found in

epidermal growth factor receptor activation by UVB [9].

act as a cocarcinogen [22].
