...
By Daniella Gray
Reporter
0
Share
Newsweek is a Trust Project member
See more of our trusted coverage when you search.Prefer Newsweek on Googleto see more of our trusted coverage when you search.
Scientists have uncovered a key way colon cancer spreads—and it may not be driven by genetic mutations as once thought.
Instead, researchers say cancer cells can change their identity, allowing them to travel through the body and form new tumors.
The findings, published in Cell Stem Cell, shed new light on metastasis—the process by which cancer moves from its original site to other parts of the body—which is the leading cause of death in colorectal cancer patients.
Read More on Health
Researchers from Weill Cornell Medicine and the Massachusetts Institute of Technology found that colon cancer cells can effectively “reprogram” themselves into a more flexible, primitive state. This shift makes them better able to survive, adapt and spread, particularly to the liver.
Dr. Tracy Proverbs-Singh, a gastrointestinal oncologist at John Theurer Cancer Center at Hackensack University Medical Center, told Newsweek that the study has "uncovered a critical reason why colon cancer is able to spread" to other organs.
She explained that the research identifies GATA6 as a kind of “guardian” that keeps intestinal cells in their proper, mature state, but when it is lost, cancer cells undergo an “identity swap,” reverting to a more primitive, fetal-like state.
"This transformation is what allows the cancer cells to break away from the original tumor, travel through the body, and form new tumors elsewhere," Proverbs-Singh said.
...
At the center of the discovery is a molecule called GATA6, which acts as a kind of “identity keeper” for cells lining the intestine. Under normal conditions, GATA6 helps cells maintain their specialized roles in the body, but when its levels drop, cancer cells can lose that identity altogether.
"We discovered that GATA6 loss acts as a critical switch," said Dr. Norihiro Goto, one of the study’s lead researchers.
Once that switch is flipped, the cells revert to a more primitive, stem-like state—similar to early developmental cells. Scientists call this ability “cellular plasticity,” meaning cells can change their type or function in response to their environment.
Proverbs-Singh said this transformation is what allows cancer cells to “break away from the original tumor, travel through the body, and form new tumors elsewhere,” effectively flipping the switch from a localized cancer to a far more dangerous metastatic disease.
This matters because these more flexible cells are better equipped to survive outside the original tumor, enter the bloodstream and establish new tumors elsewhere in the body.
Crucially, the study suggests this transformation is not primarily caused by DNA mutations, but by epigenetic changes, which turn genes on or off without altering the genetic code itself. That distinction could have major implications. For years, scientists have searched for specific mutations that trigger metastasis in colorectal cancer, but no clear driver has been found.
This new research suggests that focusing on how genes are regulated rather than on changes in them may be key.
To investigate the process, the team used advanced laboratory models known as organoids—tiny, three-dimensional clusters of cancer cells grown to mimic tumors. By repeatedly transplanting these cells in mice, the researchers were able to track how cancer cells evolve into more aggressive, spread-capable forms.
The results showed that loss of GATA6 led to widespread reprogramming, with cells adopting different identities and gaining the ability to metastasize more effectively. Importantly, the researchers also found that low levels of GATA6 are commonly seen in tumors that have already spread—and are linked to worse patient outcomes.
...
The findings could help explain why metastatic colorectal cancer remains so difficult to treat. While primary tumors can often be removed or controlled, metastatic disease is far harder to eliminate once it has taken hold in other organs.
Proverbs-Singh said the discovery could have important clinical implications, including the use of GATA6 levels to predict which tumors are most likely to spread.
"[This] could become a new way to predict the risk of metastasis, allowing us to identify high-risk patients who may need more aggressive treatment or closer monitoring," she said.
By revealing how cancer cells gain this ability in the first place, the study opens up new potential pathways for treatment.
Perhaps most significantly, Proverbs-Singh said the findings point toward future treatments that could stop metastasis before it starts—by preventing this “identity swap” and keeping cancer cells in a less aggressive state.
While she stressed that the research is still in its early stages and based on lab models, she described it as “a major step forward” that offers a new and hopeful direction for targeting the spread of colon cancer.
Contact Newsweek editors on this story: Kara Dolman and Sam Wilson.
View 0 Comments
Submit Correction
View Editorial & AI Guidelines