Rates of colorectal cancer have been increasing among adults under the age of 50, with the American Cancer Society noting it as the leading cause of cancer death in men and the second leading among women in this age group. Scientists have been investigating potential causes, and researchers may have inadvertently identified a possible contributor.
A research team, led by the University of California San Diego, has discovered that the bacterial toxin colibactin may play a role in causing colorectal cancer. Published in the journal Nature, their findings suggest that exposure to colibactin during childhood, produced by certain strains of the bacteria E. coli, can lead to mutations in the DNA of the colon. These mutations potentially elevate the risk of developing colorectal cancer before reaching age 50.
The study’s lead author, Ludmil Alexandrov, who is a professor in the Department of Cellular and Molecular Medicine at UC San Diego and a member of the UC San Diego Moores Cancer Center, stated that the research initially aimed to broadly explore colorectal cancer. However, unexpectedly, the team found differences in cancer cells between younger and older patients.
The toxin colibactin has the ability to mutate DNA in colon cells, creating conditions more conducive to cancerous growth. According to Alexandrov, exposure to this toxin during childhood can cause thousands of DNA mutations, setting the stage for cancer development at an earlier age. The research team discovered that specific DNA mutation patterns left by colibactin were 3.3 times more common in those under 40 with early-onset colorectal cancer, compared to patients diagnosed after 70. More than half of all cancerous mutations across ages could be traced back to this bacteria.
Colibactin is found in certain E. coli strains, a group of bacteria capable of causing infections in various parts of the body. While some E. coli strains cause sickness, many people may carry the bacteria asymptomatically. The most recognizable illness, diarrhea, is often spread through fecal-oral transmission, undercooked or raw meat, unwashed fruits and vegetables, or unpasteurized milk, cider, or juice. The presence of E. coli, including those producing colibactin, does not inherently guarantee the development of cancer.
Alexandrov suggests that lifestyle changes in younger generations, such as increased cesarean births, rising antibiotic use, decreased breastfeeding, and higher consumption of ultra-processed foods, might increase exposure to E. coli and colibactin, potentially affecting gut microbiome development and increasing bacterial susceptibility. As a result, early mutations might occur at the age of five in children rather than 35, providing more opportunity for cancer to develop.
Despite the challenges of detecting the presence of this bacteria and its mutation-causing potential, the discovery holds promise for aiding early cancer detection. Alexandrov’s team hopes to develop a stool test to identify individuals harboring DNA mutations from colibactin, allowing healthcare providers to assess cancer risk better. Early detection significantly improves colorectal cancer outcomes. The development of such a test, however, is expected to take a couple of years.
In the interim, the research emphasizes the importance of awareness regarding potential symptoms and encourages prompt medical consultation. Alexandrov highlights that childhood factors may impact long-term health, influencing even adult diseases like cancer.
This study has appeared on Fortune.com and provides valuable insights into the underlying causes and potential prevention of early-onset colorectal cancer.
