Bacteria silently initiate colorectal cancer children

According to a groundbreaking study published in nature yesterday, a common bacterial toxin may be the culprit for early colorectal cancer in young adults.

Scientists have identified a toxin called Colibactin, which is produced by certain strains of E. coli in the colon because it may trigger genetic changes, which can cause symptoms of cancer for decades.

“These mutation patterns are a historical record in the genome, and they point to the driving force behind early exposure to early onset diseases,” said study senior author Ludmil Alexandrov.

Once it mainly affects the elderly, colorectal cancer has become increasingly common among people under the age of 50, and has roughly doubled every decade over the past 20 years. If the trend continues, it is expected to be the leading cause of cancer deaths in young people by 2030.

An international team led by researchers at the University of California, San Diego analyzed 981 colorectal cancer genomes from patients in 11 countries with varying risk levels in 11 countries. They found that among patients diagnosed before the age of 40, the pattern of DNA mutation associated with colaglobin was 3.3 times higher than that of patients diagnosed at the age of 70.

What makes this discovery particularly worrying is how the damage begins.

“If someone gets one of the driver mutations at the age of 10, they may develop colorectal cancer decades ahead of time, and at the age of 40 instead of 60,” Alessandrov explained.

Young people with colorectal cancer usually have no family history of the disease and have few known risk factors that confuses doctors about the surge in cases. This study provides the first substantial evidence for potential environmental reasons.

The team found that mutations associated with Colibactin accounted for about 15% of the so-called APC-driven mutations, the earliest genetic alteration that directly promoted cancer development.

“When we started the project, we were not going to focus on early-onset colorectal cancer,” said Marcos Díaz-Gay, a former postdoctoral researcher in Alexandrov’s lab. “Our initial goal was to examine the global model of colorectal cancer to understand why some countries have a much higher rate than others. But one of the most interesting and compelling findings when we mined the data was the frequency of mutations associated with Colibactin in early cases.”

These findings also reveal geographic patterns, with some countries (especially Argentina, Brazil, Colombia, Russia and Thailand) showing an increase in specific mutational traits, suggesting that local environmental factors may play a role.

“Different countries may have different unknown reasons,” Díaz-Gay said.

The team is now investigating how children are exposed to garycin bacteria and whether certain dietary or lifestyle factors can increase risks. They are also developing early detection tests to analyze fecal samples of mutations associated with colon cancer and to explore whether probiotics can eliminate harmful bacterial strains.

Alexandrov notes the wider impact on cancer research: “This reshapes our perception of cancer. It may not be just what happens in adulthood – directors may be affected by events in their early life, maybe even in the first few years.”

The research is part of the Cancer Challenge Team Mutographs, a global effort funded by Cancer Research UK, which decodes patterns of DNA mutation caused by environmental exposure and lifestyle behavior.