Using a genomic analysis, a group of international researchers has identified a specific mutation responsible for an impressive rise in the risk for testicular cancer.

The mutation is really a single-base change to the genetic code that affects the game from the p53 protein that is accountable for controlling the activity of a large quantity of genes, including those responsible for protection from UV rays C based on the team\’s report within the journal Cell.

“Knowing the inherited genetics of cancer has great potential in medicine,” said study author Gareth Bond, a researcher at Oxford University\’s Ludwig Institute for Cancer Research. “It may aid the development of tests to predict the chance of developing particular malignancies. Additionally, it may tell physicians about the likely prognosis of cancers, and inform therapeutic choices, improving control over the disease.”

About half of all cancers are associated with mutations within the p53 gene. Since the p53 protein activates an array of cancer-related signaling pathways, the study team hypothesized that cancer risk could be linked to genetic variations for p53-binding sites.

The single-based change, known as a single nucleotide polymorphism (SNP), was discovered after the team analyzed genetic databases containing nearly 63,000 SNPs in search of mutations affecting p53’s capability to turn on its target genes. They could find one particular mutation that\’s very strongly linked to the risk of developing testicular cancer.

The SNP was discovered in the genetic code for any p53 response element that codes for any protein named KIT ligand (KITLG).

“It appears that this particular variant permits testicular stem cells to develop in the presence of DNA damage, when they\’re supposed to stop growing, since such damage can result in cancer,\” said study author Douglas Bell of america National Institute of Environmental Health Sciences.

Next, they performed an evolutionary genomic analysis that says other SNPs that alter p53’s ability to bind its receptors have been lost by natural selection. The KITLG mutation not just slipped with the cracks, it\’s been “positively selected within the Caucasian gene pool.”

To explain why evolutionary forces would select for any cancer-causing mutation, the research authors noted that p53 is activated in certain cells of your skin after exposure to UV radiation, fueling the secretion of KITLG and causing pigment-making cells to multiply, increased melanin production. The result is an epidermis tan that protects from future exposure to the sun\’s rays.

“During the period of evolution, as humans migrated from Africa in to the dimly lit terrain of the north, they developed lighter skin, probably to adjust to the low amounts of sunlight,” Bond explained. “Unfortunately, that adaptation also left their skin susceptible to UV damage. It is intriguing to speculate that the better form of the KITLG p53 response element is evolution’s compensation for that vulnerability. But it appears to come in a cost-which is really a greater risk for testicular cancer.”

“I’d speculate that serious sun-damage to skin might have posed a mortal threat to the early ancestors,\” he added.