Common foodborne E. coli linked to higher colorectal cancer risk in patients with hereditary polyps
Japanese study finds colibactin-producing E. coli in polyps of Familial Adenomatous Polyposis patients associated with more DNA damage, inflammation and a threefold increase in cancer diagnosis
Researchers in Japan report that a toxin-producing strain of E. coli commonly spread through contaminated food and water was found in colon polyps of patients with Familial Adenomatous Polyposis (FAP) and was associated with a marked increase in colorectal cancer diagnoses.
In an analysis of 75 patients with FAP, investigators identified colibactin-producing E. coli (pks+) in polyps and found that patients whose polyps harbored the bacterium were more than three times as likely to have developed colorectal cancer than those without it. Polyps containing the bacteria also showed higher levels of DNA damage and inflammation, findings the authors said could accelerate cancer development in people already genetically predisposed.
FAP is an inherited condition caused by a mutation that effectively removes regulatory controls on cell division in the colon, producing hundreds of polyps and creating a high baseline risk for colorectal cancer. Colibactin, the molecule produced by pks+ E. coli, is a potent genotoxin known to cause DNA breaks; laboratory studies have shown it can induce mutations in colon cells.
The bacterium spreads through contaminated food and water, and some estimates reported in media accounts put annual exposure in the tens of thousands. The new analysis focused on a high-risk, genetically defined patient group rather than the general population, and the authors framed their results as evidence that bacterial genotoxins can interact with host genetic vulnerability to promote cancer.
Colorectal cancer traditionally has been viewed as a disease of older adults, but incidence among people in their 20s, 30s and 40s has been rising in several countries, including the United States and the United Kingdom. Researchers and clinicians have been investigating environmental, dietary and microbial factors that might contribute to the trend; this study adds data about a specific bacterial mechanism that may accelerate tumorigenesis in susceptible tissue.
The analysis measured markers of DNA damage and inflammation in resected polyps and compared the presence of pks+ E. coli with clinical outcomes. The sample size was modest, and the authors noted that the findings pertain to FAP patients, who have a rare, strong inherited predisposition to polyps and cancer. They did not claim that the presence of pks+ E. coli alone causes colorectal cancer in people without such genetic risk.
Experts not involved in the study said the work reinforces growing interest in the role of the gut microbiome and specific microbial toxins in colorectal carcinogenesis, particularly how microbial factors may interact with host genetics. They also called for larger, prospective studies to evaluate whether similar associations exist in broader patient populations and to clarify potential public health implications.
The study adds to a body of laboratory and clinical research implicating bacterial-produced genotoxins in DNA damage within the colon. It suggests a biological pathway by which frequently encountered microbes could accelerate cancer development in genetically vulnerable tissue, but further research will be needed to determine the extent to which those mechanisms operate in the general population and to inform any changes in screening or prevention strategies.