Toxin caused by common stomach bug could be driving up rates of bowel cancer

Rates of bowel cancer among young Britons have been increasing for years (Picture: Getty Images)

A toxin produced by E. coli – the troublesome bug that causes vomiting and fevers – could be behind rising bowel cancer rates.

The disease, also called colorectal cancer, predominantly impacts people over 50 though for the last two decades has begun to impact more young people worldwide.

Many of these countries are richer nations in the west – including England – with poor diet, obesity and eating too much meat among the risk factors.

But exposure to a toxin produced by the bacteria E. coli could also be a factor, researchers revealed today.

Exposure to colibactin as a child can mess up the genetic signature on the DNA of bowel cells, which may increase the chance of developing bowel cancer when younger than 50, a study published today found.

This changes people’s digestive tracks and raises the risk of tumours forming, the researches said, with traces of colibactin found lurking in tumours from patients under 40.

The research, led by the University of California San Diego (UCSD) and published in the journal Nature, saw experts examine 981 bowel cancer genomes from patients with both early and late-onset disease in 11 different countries.

Colibactin’s specific pattern of DNA mutations were 3.3 more common in early-onset bowel cancer cases (in adults under 40) than in those diagnosed after the age of 70.

‘These mutation patterns are a kind of historical record in the genome, and they point to early-life exposure to colibactin as a driving force behind early-onset disease,’ said senior author, Ludmil Alexandrov, a professor at UCSD.

They also found that colibactin-related mutations account for around 15% of APC driver mutations, one of the first genes to go haywire in bowel cancer.

First author Marcos Diaz-Gay, a former postdoctoral researcher, said: ‘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.’

There are many strains of the bacteria, Escherichia coli, often just called E. coli (Picture:Getty Images)

The work is part of Cancer Grand Challenges team Mutographs, funded by Cancer Research UK.

The director of Cancer Grand Challenges, Dr David Scott, said the colibactin that seems to be affecting bowel cancer is only produced by some strains of E. Coli.

There are many kinds of E. coli, the bulk harmless to humans and are part of a smooth-running intestinal tract. One strain, known as Shiga toxin-producing E. coli, can be found wriggling in the insentiences of cows and find themselves in faeces, containing farm soil.

The strain that coughs out colibactin is not linked to infection such as diarrhoea in some people, the study said.

‘It’s unclear how the exposure originates, but we suspect that a combination of factors – including diet – may intersect during a crucial phase in the development of the gut microbiome,’ said Dr Scott.

‘This study adds an important piece to the puzzle of early-onset cancers, but it isn’t conclusive, and more research will be needed to establish a definitive link between colibactin and an increased risk of early-onset colorectal cancer.’

Sciensits pinpointed the toxin to a strain of E. coli that doesnt cause diarrhea (Picture: Getty Images)

Professor Sir Mike Stratton, Mutographs team lead and senior group leader at the Wellcome Sanger Institute, said: ‘Our research has allowed us to generate the hypothesis that the presence of colibactin leads to an increased number of mutations in colon cells, which then causes a greater risk of colorectal cancer at an early age.

‘If this turns out to be correct, we can explore preventive measures such as tests that tell us if the toxin, or the bacterium that makes it, is present, and finding ways to eliminate them from our bodies at a young age.

‘We know that diet and lifestyle choices drive the risk of developing colorectal cancer, but this study has opened up a new and exciting route we can take when researching how to lower the rate of early-onset colorectal cancer.’

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