CORNELL (US) — Scientists have identified a gene that when combined with a folate deficiency increases the risk of colon cancer in mice.
Colorectal cancer is the second leading cause of cancer-related deaths in the United States. More than 50,000 people die each year from colon cancer, many due to a lack of early detection.
The study, published in the journal Cancer Research, indicates that the SHMT1 gene may be a factor in itself, and also demonstrates how dietary folate, a B vitamin, may interact with an individual’s genetic make-up to increase colon cancer risk.
A previous study found that the same gene is a cause of neural tube defects, a common class of birth defects.
“Nutrition and genetics work together to contribute to the creation of cancer cells, and based on the similarity of folate metabolism in mice and humans; it is likely that this gene is associated with human colon cancer,” says Patrick Stover, professor of nutritional sciences at Cornell University.
Interactions among nutrients and genetic factors play an important role in the development of numerous cancers, including colorectal cancer.
“Molecular antecedents that promote development of sporadic colon cancer include DNA damage. Lack of critical nutrients (such as folate) increases rates of DNA damage. Therefore, lack of folate has the potential to induce this damage that ultimately results in the progression of colon cancer risk,” Stover says.
While screening for colorectal cancer is recommended to all individuals over age 50; close to 40 percent of the U.S. population in this age group aren’t tested.
Individuals who choose not to pursue colonoscopies may want to ensure that their diets contain adequate amounts of folate, Stover says. The U.S. recommended daily allowance for folate is 400 micrograms per day. Foods that are rich in folate include many fruits and vegetables, grains, legumes, nuts, and seeds.
The study was supported, in part, by the U.S. Public Health Service.
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