
Childhood exposure to bacterial toxin may be triggering colorectal cancer epidemic among the young
On Apr. 23, 2025, researchers from the Wellcome Sanger Institute, University of California San Diego and their collaborators announced they had found a potential microbial culprit behind the alarming rise in early-onset colorectal cancer.
The team analysed 981 colorectal cancer genomes from patients with both early- and late-onset cancer across 11 countries with varying colorectal cancer risk levels.
The study, published in Nature, reported that exposure to colibactin in early childhood imprints a distinct pattern of change, known as the “mutational signature”, on the DNA of colon cells — one that may increase the risk of developing colorectal cancer before the age of 50.
Despite overall colorectal cancer cases decreasing, this particular cancer is on the rise amongst young people in at least 27 countries. If current trends continue, colorectal cancer is projected to become the leading cause of cancer-related deaths among young adults globally by 2030.
This current study originally sought to understand the variation of colorectal cancer incidences between countries by sequencing colorectal cancer genomes from 11 countries on four continents to understand how changes in DNA contribute to geographic and age-related differences in cancer rates. However, when analysing the data, the researchers revealed interesting findings about the early-onset cases in particular.
The findings show that colibactin, a toxin produced by E. coli, leaves behind specific patterns of DNA mutations that were 3.3 times more common in early-onset cases – specifically in adults under 40 – than in those diagnosed after the age of 70. These mutation patterns were also particularly prevalent in countries with high incidence of early-onset cases.
In the study, the team also found that colorectal cancers from specific countries — particularly Argentina, Brazil, Colombia, Russia and Thailand — showed an increase in certain mutational signatures. This suggests that local environmental exposures may also contribute to cancer risk.
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Source: Wellcome Sanger Institute
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