UVB Induced Mutation of p53 in Non Melanoma Skin Cancer

Authors

Raizy Berger, Touro College

Abstract

There is a clear correlation between excessive sun exposure and the development of skin cancer. UVB radiation from the sun is potent, and as the ozone layer gets depleted, more UVB can reach Earth and cause cell damage. UV radiation causes DNA lesions, such as 6-4 photoproducts and cyclobutane pyrimidine dimers. Cyclobutane pyrimidine dimers are more abundant and take longer to be repaired and therefore are responsible for most of the mutation and DNA damage. These DNA lesions lead to mutation of the p53 gene. The signature mutation on p53 from UV radiation is a CC to TT mutation, which generally occurs at the binding site of p53. As a result, of the mutation, p53 is inactivated and can no longer perform its tumor suppressive functions. As a result, cancerous or damaged cells in the skin can proliferate and form tumors. P53 is an early step in skin carcinogenesis, and p53 mutation is found in abundance in actinic keratosis, a precancerous lesion of Squamous Cell Carcinoma. Experiments conducted on mice prove the effectiveness of sunscreen. Mice treated with UVB blocking sunscreen had significantly decreased percentage of mutation, compared to mice without the sunscreen.

Recommended Citation

Berger, R. (2018). UVB Induced Mutation of p53 in Non Melanoma Skin Cancer. The Science Journal of the Lander College of Arts and Sciences, 12(1). Retrieved from https://touroscholar.touro.edu/sjlcas/vol12/iss1/13