New research published in the journal Cancer Prevention Research has established a link that may explain why individuals who consume high-fat diets have an increased risk of colon cancer.
Researchers at Temple University compared colon tissue in non-colon cancer patients with normal colon tissue in patients with the disease. In the normal tissue from patients with colon cancer, they found that epigenetic marks on genes involved in breaking down carbohydrates, lipids and amino acids that are abundant in the fatty Western diet appeared to have been retrained. Epigenetic marks are chemical modifications that serve as on/off switches for many genes.
“These foods are changing the methylation patterns on a person’s insulin genes so that they express differently, pumping out more insulin than the body requires," the researchers said. “In people that have colon cancer, their glucose metabolic pathways and insulin signaling pathways are running at completely different levels than people who don’t have colon cancer."
The researchers not that that people don’t usually get colon cancer until the age of 50 or older, so it is unclear when the epigenetic modification of the genes begins.
“The hypothesis is that the changes in the metabolic pathways happen first, and once they occur, if any kind of mutation happens that causes a cancerous polyp, you are going to feed it through this excess insulin," they said.
The study provides the first evidence of widespread epigenetic modification of metabolic pathway genes occurring in healthy colon tissue. The researchers theorize that if modification in healthy tissue could also be found in other healthy tissues in the body, they might be used to diagnose or determine the likelihood of colon cancer by through a saliva or blood test in addition to a colonoscopy.
Researchers at Temple University compared colon tissue in non-colon cancer patients with normal colon tissue in patients with the disease. In the normal tissue from patients with colon cancer, they found that epigenetic marks on genes involved in breaking down carbohydrates, lipids and amino acids that are abundant in the fatty Western diet appeared to have been retrained. Epigenetic marks are chemical modifications that serve as on/off switches for many genes.
“These foods are changing the methylation patterns on a person’s insulin genes so that they express differently, pumping out more insulin than the body requires," the researchers said. “In people that have colon cancer, their glucose metabolic pathways and insulin signaling pathways are running at completely different levels than people who don’t have colon cancer."
The researchers not that that people don’t usually get colon cancer until the age of 50 or older, so it is unclear when the epigenetic modification of the genes begins.
“The hypothesis is that the changes in the metabolic pathways happen first, and once they occur, if any kind of mutation happens that causes a cancerous polyp, you are going to feed it through this excess insulin," they said.
The study provides the first evidence of widespread epigenetic modification of metabolic pathway genes occurring in healthy colon tissue. The researchers theorize that if modification in healthy tissue could also be found in other healthy tissues in the body, they might be used to diagnose or determine the likelihood of colon cancer by through a saliva or blood test in addition to a colonoscopy.
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