IE 11 is not supported. For an optimal experience visit our site on another browser.

Why do colon cancer tumors grow so fast? Study identifies new gene that may play a role

Colon cancer is the second most deadly form of cancer and the third most prevalent in the United States.
/ Source: TODAY

A newly identified colon cancer gene may drive the disease by making the environment in the vicinity of tumors more hospitable to them, researchers say.

The gene, which appears to speed tumor growth by pumping up inflammation around it, may offer insights into lifestyle changes, as well as potential therapies, to help slow growth down, according to the report published in Nature Communications.

Colon cancer is the third most prevalent cancer in America and the second most deadly,” said the study’s lead author, Royce Zhou, an MD and Ph.D. student at the Icahn School of Medicine at Mount Sinai in New York. “We were not interested in changes in the (patient's) DNA itself, but rather modifications that occur on top of the DNA.”

More specifically, the researchers were looking at how changes in epigenetics affects tumor growth. Epigenetics is "the study of how your behaviors and environment can cause changes that affect the way your genes work," according to the Centers for Disease Control and Prevention. "Unlike genetic changes, epigenetic changes are reversible and do not change your DNA sequence, but they can change how your body reads a DNA sequence."

The researchers found that changes in the epigenetics outside the tumor could prompt changes within the cancer cells themselves.

Colon cancer studies have often relied on laboratory-grown cancer cells, which don’t allow researchers to look at how the environment around tumors affects their growth. But Zhou and his colleagues were also able to work with tumors and healthy tissue that had been excised from colon cancer patients. The epigenetic changes that the researchers discovered were only found in tumors removed during cancer surgery — not the healthy tissue or cancer cells grown in the laboratory, Zhou said. 

After being activated by inflammation in the tumor's environment,  the gene identified by Zhou and his team appeared to increase the amount of glucose available to the cancer cells. Glucose, a type of sugar, is a crucial source for energy for living organisms. The researchers also discovered that in a mouse model, when the gene was deleted, the tumor did not grow as fast.

The new findings suggest that people might be able to lower their colon cancer risk through lifestyle changes, such as keeping blood sugar levels in the normal range, Zhou said. The research also suggests that there might be a medication, an SGLT2 inhibitor that is already FDA-approved to lower blood sugar in people with diabetes, that could possibly help slow tumor growth.

“The next step would be to see whether the SGLT2 inhibitor can have a role in combatting colon cancer,” Zhou said.

The new findings suggest that the environment around a tumor may speed up cancer growth, said Dr. Michael Shusterman, a medical oncologist at NYU Langone’s Perlmutter Cancer Center and a clinical assistant professor at NYU Long Island School of Medicine.

The gene identified by the researchers “is not a classic gene we understand as having been linked to colon cancer,” Shusterman, who was not involved with the new study, said. “The gene is essentially a kind of glucose regulator.”

He agreed that the new research indicates that inflammation in the tumor’s environment may favor the development of tumors and added that people may benefit from strategies to reduce inflammation.

One way to drive down inflammation is to engage in moderate to vigorous exercise, Shusterman said, explaining that earlier research in stage 3 colon cancer patients showed that higher levels of activity were associated with a reduced incidence of tumor recurrence.

People with colon cancer might also want to steer clear of foods known to increase inflammation, such as ultra-processed foods, processed meats and red meat, Shusterman said.