People and even organizations have been debating on whether ultraviolet rays can cause skin cancer over the past years. Research and experiments on p53 genes of actinic keratosis (AK) have been carried out to determine whether sunlight acts as a carcinogen.
Ultraviolent induced mutations in the p53 genes of AKs can help in identifying when sunlight mutagenesis occurs. However, more evidence confirming whether the mutations are as a result of the prior occurrence in sun damaged skin or as an event within the AK is needed. A survey done on patients in England had base changes indicating sunlight as the mutagen 4, 5, 7 having most of the coded mutations which would alter the amino acid. The majority of patients carried multiple AKs in the same region of sunburn, but the AK s never had a common mutation. Each of the AKs mutant clones developed from an independent ultraviolet photon occurrence.
The presence of p53 mutations throughout the majority of lesions was evidence that sunlight acted as mutagen before or during AK clonally expansion. It was the first skin cancer development clinically apparent lesion. Although P53 mutations occurred before the AK, a vast number of them did not precede the AKs because AKs had various p53 mutations. In a case where AKs would arise within independent small p53 mutant clones, a non-AK cell would surround the AK containing the similar p53 mutation.
To determine the purpose of p53 in normal skin, wild mice were irradiated on the back with different doses of ultraviolet B. A day later, there was a presence of sunburn cells in the epidermis and the cells increased with increase in ultraviolet B dosage. The appropriate nature of sunburn cells was confirmed by assaying for DNA strand breaks in keratinocyte nuclei by using fluorescent in situ end-labeling. P53-/- animals had a lesser scope of induction compared to p53+/+.However, doses that were used in the mice experiment are 1 and two as much as those necessary to cause a noticeable erythema in human beings.
Sunlight triggered mutation phenotype should reflect in early occurrence.P53 which are a transcription factor with targets that in cell-cycle regulation genes has proven to take part in DNA surveillance route that monitors the genome for damaged DNA. This path terminates the aberrant cell rather than restoring the genome resulting to sunburns. The dying cells as a result of sunburn are different from swollen cells of necrosis and are seen after irradiating the mammalian skin with ultraviolet A, B or C. Sunburn cells appear to be crucial in countering skin cancer as they occur in the cell type of source for skin tumor keratinocytes and result from DNA damage caused by ultraviolet radiation. Sunburn cells have now proven to depend majorly on the p53 gene which occurrence of tumors in mouse skin and mutates in most cancer and precancerous human skin cells.
Ultraviolet rays can be a tumor promoter in mouse and human skin just like other tissues that damage DNA. The results can multiply the number of mutant cells without even needing a mutator phenotype. Mutation in the p53 gene causes by sunlight can account for the salient qualities of human skin carcinogenesis. Individuals who sunburn are more exposed to skin cancer that those of Celtic descent.
In conclusion, from the experiments and survey research done, ultraviolet rays have proved to be carcinogenic. In the experiment, sunburn cells are primary causes of skin tumors. The majority of people expose to skin cancer are those who sunburn as the damaged cells have effects on DNA and cell mutation.
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