The role of p53 in sunburn.
To help understand the function of p53, described above by CrazyIvan, it is useful to employ an example.
UV radiation is a powerful carcinogen, and when our skin is exposed to this radiation, the DNA in the skin cells is damaged at random points.
As CrazyIvan has explained, when DNA is damaged, the p53 gene is upregulated. This causes the cell to undergo programmed cell death, otherwise known as apoptosis.
When many skin cells are damaged through exposure to UV radiation, this mass apoptosis is manifested as layers of dead skin that you can peel off in nice large chunks. (see the art of peeling large pieces of skin delicately)
Consider the fact that you have 2 copies of the p53 gene in each cell, which is represented as p53+/+. Now, suppose one copy of p53 is damaged in some of the cells (p53+/-). The next time you go and get sunburnt, the apoptosis of the p53+/- cells is less efficient, but usually still goes ahead. However, if you damage the DNA of a p53+/-cell, and it happens to knock out the second copy of p53 in one or more of your skin cells, things can start to get very dangerous.
p53-/- cells do not undergo apoptosis. This does not mean it is now a cancerous cell, but rather a cell without emergency brakes. p53-/- cells are genetically unstable and are more prone to tumours. If you were to get sunburnt a third time, and damage the DNA in a p53-/- cell, the cell would be unable to self destruct. If this mutation activates an oncogene, the result is a cancerous cell.
Because of the way p53 functions, it is often referred to as a tumour suppressor gene, or the “guardian of the genome”.
Now you should have a fair idea of how to quickly and efficiently induce basal cell carcinomas.