Radiation Induced Skin Cancer

Radiation Induced Skin Cancer

Slide 2

Categories of UV Rays

The frequent risk factor in developing the non-melanoma cancer is the excessive exposure to ultra violet radiation from sunlight. The ultraviolet radiations are carcinogenic in nature. They start as well as promote the phenomenon of carcinogenesis; a process converting the normal cells into cancerous. Moreover, carcinogenesis is the production of novel cells of cancer. Ultra violet radiation stimulates the tumor forming mediators such as protein kinase C in human beings and mice.

The spectrum of ultra violet radiation exists between X-rays and visible region. The ultra violet radiation has further three subdivisions that include UVA, UVB and UVC. The wavelength range of UVA is 315 to 400 nm and of UVB is 280 to 315 nm. According to Wheeler et al, these two categories are more likely to cause squamous cell carcinoma, as they are the carcinogenic electromagnetic radiations (Wheeler et al, 2004).

Slide 3

Carcinogens Produced by UVR

The category B of UVR involved in damaging the DNA directly. UVB possesses the wavelength of 280 to 315 nm. UVB stimulates the generation of carcinogenic photoproducts such as Dewar photoisomer, pyrimidine pyrimidone dimer, and cyclobutane pyrimidine dimer. Out of these carcinogenic constituents, the cyclobutane pyrimidine dimer is the main photoproduct affecting about 85 percent of DNA via causing primary lesions in DNA.

Slide 4

Mutations in DNA

When DNA affected by UVB replicates through one of the two types of mutations; tandem double mutations and transition mutation. Mutation is the enduring change within the sequence of DNA gene. Mutation alters the sequence of the gene in DNA for the synthesis of required protein. The locations of these mutations, in case of skin cancer, are sites of dipyrimidine on DNA. These two mutations are common in the squamous cell carcinoma induced by ultra violet radiations.

Slide 5

Mutations in Squamous Cell Carcinoma

The discussed two types of mutations are common in skin cancer related to both; mice and human being. Many types of gene mutations occur in case of skin cancer by UV rays, but transition and tandem double mutations are more common. Both the mutations occur at p53 gene. The induction of p53 protein also causes the sunburn following mutation. When these mutated sunburn cells get further exposure to UV rays, it initiates the formation of squamous cell cancer. UVR affects the gene expression involved in oncogenesis, cell growth, cell differentiation, and inflammation.

Slide 6

Role of Protein Kinase C

The over expression of protein Kinase C epsilon in skin epidermis of mice increases the sensitivity of skin to ultra violet radiation. This sensitization induces damage in skin leading to the squamous cell carcinoma. Protein Kinase C epsilon is the major element promoting the skin tumor. It promotes the production of 12-O-tetra decaoylphorbol-13-acetate. Moreover, certain other stress such as UVR also stimulates this tumor promoter.

Slide 7

Mice before Exposure to UV Light

In order to evaluate the role of PKC epsilon in inducing the skin cancer, the investigators crossbred the SKH-1 hair less mice with transgenic hairless ...