Colorectal cancers with a specific DNA damage pattern linked to colibactin-producing bacteria show more widespread changes in their genome compared to cancers without this pattern.

Colorectal cancers with colibactin-related DNA damage patterns show the same levels of overall mutations and known cancer-causing gene changes as other colorectal cancers, suggesting colibactin causes cancer through a different biological mechanism.

Certain strains of E. coli that produce a toxin called colibactin are linked to a specific pattern of DNA damage found in colorectal tumors. This DNA damage pattern is more commonly found in tumors from people diagnosed with colorectal cancer before age 55 compared to those diagnosed at age 59 or older.

When human colon tissue grown in the lab is exposed to a specific type of E. coli that produces colibactin for three months, it develops a unique pattern of DNA damage that matches the pattern seen in human colorectal cancers.

Researchers found that DNA damage patterns linked to a specific bacterial toxin were present in 39% of colorectal tumors from individuals with APC gene variants, compared to 11% in individuals without these tumors. This suggests a statistical relationship between the bacterial toxin and the type of DNA damage observed in these cancers.

DNA damage caused by the bacterial toxin colibactin is found in the earliest genetic changes in colorectal cancer, suggesting that exposure to this toxin happens early in life and helps create the initial mutations that lead to cancer.