Rise of colon cancer in young people linked to childhood exposure to this bacteria: study

A groundbreaking new study suggests that a gut-dwelling bacteria may be behind the recent surge in early-onset colorectal cancer cases.

The potential culprit? Colibactin, a toxin produced by certain strains of E. coli that thrive in the colon and rectum.

“We believe this exposure occurs very early in life — likely during the first decade — when children are infected,” Dr. Ludmil Alexandrov, senior study author and a professor at the University of California San Diego, told The Post. 

An alarming surge

Once thought of as a disease that strikes later in life, colorectal cancer is now on the rise among young people in at least 27 countries. 

In the US, the number of people under 55 being diagnosed has nearly doubled over the past decade, and more people are dying from the disease each year, according to the American Cancer Society. 

“Until now, prior studies had not been able to identify a clear cause or even distinguish early-onset cases from those diagnosed later in life,” Alexandrov said. “Our study helps change that.”

A bug with a bite

In the study, Alexandrov and his colleagues examined cancer genomes from patients with both early and late-onset colorectal cancer across 11 countries. 

The team found that this bacteria, colibactin, leaves behind a distinct DNA fingerprint on colon cells when kids are exposed to it. These mutations were 3.3 times more common in early-onset cases than in those diagnosed after the age of 70. 

Colibactin-linked mutations show up at the early stages of tumor development, they found, often within the first 10 years of life. 

“While the infection is transient, the damage it causes can persist for decades,” Alexandrov said. 

Even more alarming: The study found that about 15% of APC driver mutations — some of the earliest genetic changes that directly promote cancer development — were linked to colibactin.

“If someone acquires one of these driver mutations by the time they’re 10 years old, they could be decades ahead of schedule for developing colorectal cancer, getting it at age 40 instead of 60,” Alexandrov said. 

Is this the only reason colorectal cancer is on the rise?

The jury is still out on whether colibactin is the main driver behind the rise of early-onset colorectal cancer cases, or just one factor among many. 

“Colibactin likely plays a key role in driving early-onset colorectal cancer, though other factors — such as diet, inflammation and genetics — are also likely contributors,” Alexandrov said.

“Still, the scale of colibactin’s impact in our study was striking, and it stands as the first clearly identified factor linked to the rising of early-onset colorectal cancer,” he added. 

How are children exposed to this bacteria?

Alexandrov explained that exposure to colibactin occurs “through colonization by E. coli — typically through the gut, and often without any obvious symptoms.”

Additionally, the study uncovered varying mutational patterns in colorectal cancers from countries like Argentina, Brazil, Colombia, Russia and Thailand, suggesting local environmental exposures could influence cancer risk.

“It’s possible that different countries have different unknown causes,” said Marcos Díaz-Gay, study first author and a former postdoctoral researcher in Alexandrov’s lab.

“That could open up the potential for targeted, region-specific prevention strategies,” he added.

What this discovery means for catching cancer in the future

The study sets the stage for two key areas of research.

First, Alexandrov wants to develop a test that can detect colibactin-induced mutations in order to identify people exposed in childhood who might be at an increased risk for early-onset colorectal cancer.

“This could enable regular monitoring and earlier detection, improving their clinical outcomes,” he said. “We hope to have a working version of this test within two to three years.”

Second, Alexandrov and his team are exploring ways to prevent early-life exposure.

“While the exact causes are still unclear, possible factors include mode of birth, breastfeeding, antibiotic use and consumption of ultra-processed foods,” he said. 

“We’re also investigating whether targeted probiotics could help prevent colonization by colibactin-producing bacteria.” 

Both research efforts will take time, but Alexandrov is hopeful that they will make meaningful progress and develop more practical approaches within the next five years.

His final message: “What happens in early childhood can have lasting effects on our health many decades later.”

“In this study, we show how a childhood bacterial infection may increase the risk of developing colorectal cancer as a young adult. But this may be just one example,” Alexandrov said. 

“It’s very likely that other early-life environmental exposures or infections could similarly leave long-term biological footprints with substantial impacts on long-term health.”