New research shows that childhood exposure to bacterial toxins may play a key role in the global rise in early onset of colorectal cancer.
The study, published April 23rd in Nature, found that a toxin called colibactin, produced by certain strains of E. coli that live in the colon and rectum, can alter DNA.
Researchers at the University of California reported that early exposure to colibactin leaves a unique mark in colon cell DNA.
However, it is important to note that this study did not prove that colibactin caused cancer, and only identified a link between toxin-related mutations and early-onset disease.
“These mutation patterns are a type of historical record of the genome, pointing to early exposure to colibactin as the driving force behind early onset disease,” says Ludmil Alexandrov, professor of the Department of Cell and Molecular Medicine at the University of California, San Diego.
“If someone gets one of these driver mutations by the age of 10, it could be decades ahead of the expected development of colorectal cancer, and you'll get it at age 40 instead of age 60,” he said in a media release.
Colorectal cancer includes two types of cancer: colon cancer and rectal cancer.
Generally, it spreads more slowly than many other cancers, often remaining in the colon or rectum for months or years before spreading elsewhere. This means that treatment is usually very effective if detected early.
The incidence of colorectal cancer among older adults has declined, but they have been climbing people under the age of 50 in Canada and around the world over the past decades.
If the current trend continues, it is predicted to be a leading cause of cancer-related deaths in young adults by 2030.
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“The fastest growing subset of the population who suffer from colorectal cancer and primarily suffer from rectal cancer is between the ages of 28 and 39,” said Barry Stein, president and CEO of Colorectal Cancer Canada.
“And there's no reason to understand why these people are diagnosed or why they have colorectal cancer in the first place.”
The question of why this is happening is why researchers at the University of California have delved deeper into it. Stein explained that there is already some evidence linking enterobacillus to colorectal cancer, whether it is due to it or just a correlation, and said the study would add another part to the puzzle.
To explain the medical mystery, the researchers in this study examined 981 colorectal cancer genomes from patients with both early-onset and late-onset disease in 11 countries with different risk levels for colorectal cancer (including Canada).
The researchers found that colibactin leaves a DNA mutation pattern in colorectal cancer, 3.3 times more common in adults diagnosed before age 40 than those diagnosed after 70 cases.
Previous studies, including previous studies from Alexandrov's lab, have discovered colibactin-related mutations in about 10-15% of all colorectal cancer cases.
BU, these studies focused on late-onset cases or did not distinguish between early-onset and late-onset disease. The latest study is the first to specifically highlight a significant increase in colibactin-related mutations in early-onset cases, the researchers said.
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Researchers have discovered that the damage caused by colibactin appears to kick surprisingly quickly. By analyzing the molecular “timing” of various DNA mutation patterns, we were able to demonstrate that colibactin-related mutations tend to appear early in the tumor developmental process, often in the first decade.
This means that colibactin-producing bacteria are colonizing the child's digestive system early on, and may quietly change DNA in ways that could increase the risk of developing colorectal cancer throughout the lifetime, long before warning signs appear.
Dr. Ohnojima, chief of the Molecular Pathological Epidemiology Program at Brigham and Women's Hospital in Boston, called the findings “attractive.”
“Cancer occurs in a long-term process. So people are 40, 45, or 60 years old and have cancer. They have symptoms and go to the doctor,” he said. “But in reality, the process can start earlier. We don't know when it will start yet, but it can start pretty early, like a baby.”
And that's what the research points out, he added.
Stein said it's premature to tell, but that if there is a link between bacteria and colorectal cancer, it has “a very profound effect.”
“For example, these may be things you can look for when you're screening for diseases in terms of preventing them in the first place,” he said. “Or alternatively, through treatment, they can attack these types of bacteria through vaccine development and drug development.
In the meantime, researchers say there is much we still don't know – and this discovery opens the door to a whole new set of questions.
How are children exposed to colibactin-producing bacteria? Also, are there any ways to reduce or prevent that exposure? Are certain dietary, environmental, or lifestyle factors making the body more kinder than these microorganisms? And how can someone even know if they already have these kinds of mutations?
The team is actively digging into these questions. They are investigating a variety of theories, including whether probiotics can help safely wipe out harmful strains.
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