Inflammation in the gut is typically treatable, but new research suggests it can leave lasting marks on cells – with potential consequences for cancer risk.
Colorectal cancer is among the most common forms of the disease, and a new study demonstrates that chronic gut inflammation may leave traces in cells that can elevate cancer risk even years later.
Research published in the journal Nature by researchers at the Broad Institute of MIT and Harvard shows that even inflammation that has long subsided can leave a lasting impact on cells. Even after tissue appears healed, some intestinal cells retain a kind of molecular memory. Experiments conducted on mice revealed that this memory can later accelerate tumor growth. This finding highlights the complex relationship between past inflammation and future health risks.
For the study, researchers induced colitis – a chronic inflammation of the colon – in mice. They continued to observe the cells long after the tissue had healed. Epigenetic markers remained present across numerous cell divisions and were passed on from stem cells to their daughter cells, creating entire cell lines that differed from healthy cells, even without any visible external changes.
When researchers then introduced a cancer-promoting mutation, a significant effect emerged: tumors grew faster and larger in tissue with this inflammatory history compared to tissue without prior inflammation. Certain genes, including those that promote cancer growth, were more easily activated.
The key lies in what’s known as the epigenome, which controls which genes can be activated in a cell. Inflammation alters this control in the long term, making cells more susceptible to cancer. Understanding the epigenome is crucial for understanding how environmental factors can influence disease development.
“This finding is a prime example of how our experiences and exposures shape our future health,” said study leader Jason Buenrostro of Harvard University. “We’ve shown that epigenetic changes are the missing piece in understanding how inflammation leads to cancer.”
The results may also assist explain the increasing incidence of colorectal cancer in younger people. Factors like diet or environmental exposures often have only temporary effects, but they apparently leave lasting traces within the body. “Your diet in your youth is not your current diet, but it can influence your cancer risk throughout your life,” said first author Surya Nagaraja.
Researchers are now investigating whether these changes can also be detected in humans, potentially through stool samples. This could help identify individuals at higher risk. In the long term, therapies that specifically target these epigenetic processes may be possible.
It’s important to note that these are currently results from animal models. Further studies are needed to determine whether these mechanisms translate directly to humans.
