A Gene That Drives Colon Cancer
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genetic puzzle

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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For more information…

Functional characterization of age-dependent p16 epimutation reveals biological drivers and therapeutic targets for colorectal cancer
Our study demonstrated that age-dependent p16 epimutation creates a permissive microenvironment for malignant transformation of polyps to colon cancer. Our findings provide a mechanistic rationale for future targeted therapy in patients with p16 epimutation...

Gene p16 drives colorectal cancer, potential therapy target
Colorectal cancer is the fourth most common and second deadliest cancer. How colorectal cancer develops is not well understood, but a team led by researchers at Baylor College of Medicine reports in the Journal of Experimental & Clinical Cancer Research that silencing the gene p16, even though the DNA itself does not change, can drive colorectal cancer progression in animal models. The researchers also revealed a strategy that reduced tumor growth and improved survival in tumor-bearing mice, opening new possibilities for future targeted therapies in patients with gene p16 alterations...