According to the estimates of the American Cancer Society, there will be 62,480 new cases of melanoma diagnosed in the United States in 2007, and 8,420 deaths may occur due to this cancer. In the case of nonmelanoma skin cancers, including basal cell carcinoma and squamous cell carcinoma, it is estimated that around one million new cases will be diagnosed during the current year. One of the major risk factors for skin cancer is ultraviolet radiation from sunlight, though exposure to various chemical pollutants and viral infections also contributes to skin cancer incidence. Solar radiation represents the spectrum of electromagnetic radiation with wavelengths ranging from UV, visible, and infrared.
In the case of skin cancer, exposure to the UV range of solar radiation is the major etiological factor. UV light in itself can be divided into three ranges: UVC, UVB, and UVA. All three ranges of UV are capable of causing skin damage, though UVC is efficiently blocked in the outer ozone layer of the atmosphere. However, UVB and UVA reach the earth's surface and thus cause damage to skin. Overall, exposure to solar UV radiation, irrespective of UVA and/or UVB, increases the risk of developing skin cancer or accelerates skin aging.
As mentioned above, skin cancer is broadly classified into two types: nonmelanoma and melanoma skin cancers. Most of the skin cancers fall into the former category, whereas in the latter case, there is an involvement of melanocytes only, a type of skin cell that is responsible for giving pigmentation/ color to the skin. Depending upon the type of cells involved, nonmelanoma skin cancers are further classified into two types: basal cell and squamous cell carcinomas. Nonmelanoma skin cancers rarely spread to other parts of the body; however, melanoma skin cancers can spread/metastasize to other parts of the body. Actinic keratoses, as a result of chronic sunlight exposure, can also develop into nonmelanoma skin cancer, specifically SCC.
Apart from these, certain viral warts and Bowen's disease can develop into SCC, whereas clinical atypical moles can be precursors for melanoma. Most of the mortality is due to melanoma skin cancer because of its ability to metastasize, whereas more than 90% of the cases of nonmelanoma skin cancer can be cured. In today's world, with a depleting ozone level as a consequence of increased use of chlorofluorocarbons and other ozone-depleting substances, exposure to the UV range of sunlight has become a leading risk factor for developing skin cancer.
DNA damage and generation of reactive oxygen species are the two key events involved in pathogenesis of UV-induced skin cancer, though to some extent immunosuppression due to UV exposure and other factors is also involved in skin cancer etiology. For reactive oxygen species generation, the electromagnetic energy of UV light is absorbed by chromophores in the skin such as DNA, porphyrins, urocanic acid, and aromatic amino acids. These chromophores, after absorbing energy, become energized and react with oxygen molecules present in the intracellular milieu, and thus initiate the formation of reactive oxygen species.
In UV-induced DNA damage, cyclobutane pyrimidine dimers and 6-4 photoproducts are formed in the DNA strands upon exposure to UV, and these modifications in DNA lead to mutations. As far as mutagenic potential is concerned, CPDs are far more mutagenic than 6-4 pps, because the latter are more efficiently repaired. Both these photoproducts usually occur in runs of tandem pyrimidine residues often termed as "hot spots" for UV-induced mutations. These mutations, such as C~T and CC~TT in response to UV exposure, are also usually referred to as UV-signature mutations.
However, within the skin, there exists a system of nucleotide excision repair, which can normally take care of most of these deleterious mutations. There are two NER pathways: global genome repair, which repairs DNA lesions throughout the genome, and transcription coupled repair, which preferentially repairs UV-induced CPDs in the transcribing strand of DNA. Consequently, human patients with the rare hereditary disorder Xenoderma pigmentosum have increased risk of developing skin cancers, and demonstrate increased sensitivity to sunlight due to a deficiency in the nucleotide excision repair.
The other two hereditary human diseases associated with defective NER are Cockayne's disease, where patients exhibits hypersensitivity to cytotoxic as well as mutagenic effects of UV, and trichothiodystrophy, where human subjects have a defect in transcription coupled repair. In addition, there also exists a base-excision repair system to repair the damage to DNA by reactive oxygen species such as 8-oxoguanine.
Regarding the susceptibility of developing cancer apart from the hereditary disorders listed above, findings of a recent study have shown a direct correlation between sunlight exposure, eye color, red hair, and frequency and age of getting sunburns to the development of basal cell carcinoma. For preventing the development of skin cancer, efforts have been made to educate the population to minimize exposure to sunlight especially during midday hours, wear protective clothing when outdoors, and use sunscreens abundantly.
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