A new international study suggests a bacterial toxin may be driving the rapid rise in colon cancer cases among younger adults.
Researchers at the University of California San Diego say the culprit could be colibactin, a toxin produced by certain strains of E. coli commonly found in the human gut.
Published this week in Nature, the study analyzed nearly 1,000 colorectal cancer genomes from patients across 11 countries. Scientists found that colibactin leaves a unique pattern of mutations in colon cells—a genetic fingerprint that was more than three times as common in patients under 40 than in those over 70. These mutations appear to take root early in life, likely during the first decade, when exposure to E. coli colonization is most likely to occur.
Dr. Ludmil Alexandrov, senior author of the study and a professor at UC San Diego, explained that while E. coli infections may be short-lived, the genetic damage inflicted by colibactin can persist for decades. This long-lasting impact helps explain why an increasing number of young adults with no family history or traditional risk factors are being diagnosed with colon cancer.
According to the American Cancer Society, diagnoses among Americans under 55 have nearly doubled in recent years, and deaths from the disease are climbing. If current trends continue, colorectal cancer is projected to become the leading cause of cancer-related death among young adults by the end of the decade.
Previous research had already shown that colibactin can disrupt DNA, but this new study is the first to make a strong connection between these genetic mutations and early-onset cases. Notably, around 15 percent of APC driver mutations—some of the earliest known triggers in colorectal tumor development—were linked to colibactin exposure. If a child acquires one of these mutations before age 10, researchers say they could develop cancer decades earlier than expected.
Researchers are now looking into how children are exposed to colibactin-producing E. coli. While the bacteria can be present without symptoms, potential factors may include birth method, breastfeeding, antibiotic use, and processed food consumption. The team is also exploring ways to prevent such exposure altogether. One possibility includes developing probiotic treatments to counteract harmful bacterial strains.
In addition to prevention, the team is working on a test that could detect colibactin-induced mutations in stool samples. Such a tool could help identify individuals who were exposed in childhood and allow for earlier screening and intervention. Alexandrov hopes a working version of the test could be ready in the next few years.
The study also found regional differences in mutation patterns, with countries like Argentina, Brazil, Colombia, Russia, and Thailand showing elevated colibactin-related signatures. This could point to varying environmental or dietary exposures and highlights the need for country-specific research.
While colibactin is not the only suspected factor behind the rise in early-onset colorectal cancer, its role appears to be significant. Other contributors such as diet, chronic inflammation, and genetic predispositions are still being studied. But researchers say colibactin is the first clearly identified biological agent directly tied to this growing public health concern.
The findings represent a major step forward in understanding the origins of a disease that, until recently, was largely confined to older adults. Alexandrov believes this research signals a broader shift in how we think about cancer development—that exposure to certain environmental or microbial factors in early childhood could silently pave the way for disease decades later.
“This could be just one example,” he said. “It’s very likely that other early-life infections or exposures also leave long-term biological footprints that affect our health in adulthood.”