During a disease process, our genes can be silenced which means they can't do the work they were meant to do. In colon cancer, when a gene called P-sixteen is silenced, our risk for the cancer goes up.

P-sixteen is a tumor suppressor, but the region of the gene that regulates p-sixteen can be modified or turned off by mutation.

This epimutation happens when chemical changes occur on the DNA with the addition of small chemical groups. If you remove them, the gene can be turned back on, like a switch.

So, epimutations could be targeted because they're reversible. As we age, epigenetic changes that silence p-sixteen accumulate and stops inhibiting cancer cells.

A second gene involved in colon cancer is called Apc or Adenomatous Polyposis Coli which is another tumor suppressor gene. To see how this mutation combined with p-sixteen changes affect colon cancer risk, researchers combined them the genome of one mouse.

Long term studies with these mice showed that they had more colon tumors compared to mice with just the Apc mutations. Then as the mice aged, even the healthy p-sixteen accumulated changes and both copies of the genes were then silenced. This further raised their cancer risk.

When they treated these cancer prone mice with both a drug that stops the immune suppression and a treatment to turn on p-sixteen, that worked better than either drug alone.

This study shows the important role that epimutations play in colon cancer and could lead to better treatments and even diagnoses.

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