Radiation-induced skin cancer

Albert, R.E., Burns, F.J., and Shore, R.E. (1978). Comparison of the incidence and time patterns of radiation-induced skin cancer in humans and rats, page 49 in Late Biological Effects of Ionizing Radiation, lAEA-SM-224/105, (International Atomic Energy Agency, Vienna). 

Mantena SK, Meeran SM, Elmets CA, Katiyar SK. 2005. Orally administered green tea polyphenols prevent ultraviolet radiation-induced skin cancer in mice through activation of cytotoxic T cells and inhibition of angiogenesis in tumors. J Nutr 135 2871-2877. 

Some races are more liable to be affected by toxic materials than others. Fair-skinned people are more prone than dark-skinned to chemically induced dermatitis and also to radiation induced skin cancers. 

DNA strongly absorbs UV radiation, especially mid-range UVB (290 to 320 nm) radiation. Two major DNA lesions are induced following UV exposure, pyrimidine dimers and 6-4 pyrimidine-pyrimidone photoproducts. Because the action spectrum (induction of a biological activity as a function of wavelength) for erythema closely matches the action spectrum for pyrimidine dimer formation, DNA is believed to be the chromophore for sunburn.6 Pyrimidine dimer formation, or more properly, the failure to adequately repair dimers after solar irradiation is also the primary cause of sunlight-induced skin cancer formation.7-8... 

There is now sufficient epidemiological evidence to classify arsenic as a human carcinogen and a cause of skin cancer. In people chronically exposed to toxic doses of arsenic, such cancers may be preceded by discolored skin (hyperpigmentation) and development of homy skin surfaces (hyperkeratosis). These areas may progress to locally invasive basal cell carcinomas or to squamous cell carcinomas capable of metastasis. Unlike skin cancers that develop on skin exposed to ultraviolet solar radiation, arsenic-induced skin cancer frequently develops in areas not commonly exposed to sunlight, such as the palms of hands or soles of feet. 

With reduced ozone levels, more ultraviolet radiation from the Sun reaches Earth. Among humans, UV-induced skin cancer and eye damage are becoming a serious threat. The increased levels of radiation also damage phytoplankton in fresh and marine ecosystems. Since phytoplankton are the base of the aquatic food chain, this damage affects all other water species. As you learned earlier, the presence of ozone close to Earth damages crops and forests. A lack of ozone in the atmosphere, however, also reduces the yield of crops, such as barley and canola, and harms forests. 

People with significant exposure to ultraviolet radiation, such as from sunlight, may also be at increased risk of developing skin cancer due to PAH exposure. Ultraviolet radiation has a synergistic influence on PAH-induced skin cancer following dermal exposure. It enhances... 

Partly as a result of epidemiological evidence it is now generally accepted that the majority of human cancers result from exposure to environmental carcinogens these include both natural and man-made chemicals, radiation and viruses. This concept follows on from many observations and work in the early part of the century which showed that coal tar, and then the aromatic hydrocarbons derived from it, could induce skin cancer in animals. Indeed, the relationship between such substances and cancer was suggested as early as the 18th century, when in 1775 Sir Percival Pott related scrotal cancer in chimney sweeps to exposure to soot and coal tar. 

If all the atmospheric ozone were compressed into a single layer at STP on Earth, that layer would be only about 3 mm thick Although the concentration of ozone in the stratosphere is very low, it is sufficient to filter out (that is, absorb) solar radiation in the 200- to 300-nm range [see Equation (17.3)]. hi the stratosphere, it acts as our protective shield against UV radiation, which can induce skin cancer, cause genetic mutations, and destroy crops and other forms of vegetation. 

Recent reports have identified the p53 genetic marker for UV-induced skin cancer (Piercell et al. 1991 Rady et al. 1992 Burns et al. 1993 Moles et al. 1993). The DNA mutations induced by UV light occur when UV radiation is absorbed by the DNA and pyrimidene photoproducts are produced. The misrepair of the photoproducts at dipyrimidine sites causes transition mutations (Mitchell et al. 1992). CC to TT transition mutations in the p53 gene have been identified as the unique molecular marker for UV-light-induced skin cancer (Brash et al. 1996) and the resulting mutation... 

Skin cancer is caused by exposure to UV radiation and the sun is the main source of this radiation. Sunscreens were initially formulated to prevent sxmbums laboratory studies later revealed that in rodents they could reduce UV-induced skin cancer which resembles human squamous cell carcinoma. Three randomised trials in older adults showed the ability of sunscreens to moderately reduce the occurrence of solar keratoses and the squamous cell carcinoma. However, no effect was observed for basal cell carcinoma [81 ]. These higher risks were found when sun exposure appeared to be intentional, that is, with the desire to acquire a tan, a healthy look or simply to spend as long as possible in the sun with as much skin exposure as possible. 

Radiation-induced cancers in humans are found to occur in the hemopoietic system, the lung, the thyroid, the liver, the bone, the skin, and other tissues. 

Albert, R.E., Phillips, M.E., Bennett P., Burns, F., and Heimbach. R. (1969). The morphology and growth characteristics of radiation-induced epithelial skin tumors in the rat, Cancer Res. 29,658. 

---