In recent years, a worrying phenomenon has emerged in the field of public health: an increasingly marked increase in colorectal cancers among young adults. If, historically, this type of cancer was considered a disease of the elderly, it now affects individuals under the age of 50. In France, as in many other countries, this trend obviously concerns researchers and health professionals, because traditional risk factors such as poor diet, sedentary lifestyle, or smoking are not enough to explain this development.
But a new scientific advance could offer an explanation: this explosion of colorectal cancers among young people could be linked to a toxin present in our intestine, produced by a common bacteria and until now often considered harmless. This toxin is called colibactin, and it could well be one of the key elements of this worrying phenomenon.
Colibactin, suspect number one
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Colibactin is a toxin produced by certain strains of Escherichia coli (E. coli), a bacteria found naturally in the human microbiota, particularly in the intestine. Although most strains of E. coli are harmless, some, such as those carrying the pks gene, are capable of producing this toxin, capable of disrupting human DNA.
In a study recently published in Nature, an international team of researchers revealed that colibactin may be responsible for the formation of genetic mutations directly linked to the development of colorectal cancer. Their research was based on the analysis of DNA from 981 colorectal tumors from patients in 11 different countries. By searching for signatures of specific mutations, scientists discovered a striking correspondence between certain genetic alterations and the presence of colibactin.
The results of this study show that the colibactin genetic signature is much more frequent in young patients suffering from colorectal cancers. In fact, the specific mutations caused by this toxin were 3.3 times more present in those under 40 than in those over 70, suggesting a direct link between the toxin and the increase in early colorectal cancers.
Exposure from childhood?
What is even more alarming is that this toxin could be present in our body from the first years of life. Indeed, researchers suspect that exposure to colibactin is not a phenomenon that develops in adulthood, but rather a process that could begin in childhood.
Colibactin has the ability to cause DNA mutations in human cells by interfering with their genetic structure. If this toxin is present in the intestine for a long time — especially during youth — it could, over time, cause mutations in the cells of the intestine, increasing the risk of colorectal cancer earlier in life. One of the worrying features of this phenomenon is that the affected person may not show any obvious signs of injury for years, making detection of the problem very difficult.
This also raises the question of whether environmental factors, such as diet, could play a role in activating these E. coli strains. coli producing colibactin. Changes in the modern diet, rich in fats and sugars, could favor the establishment and proliferation of these pathogenic strains, thus increasing the risks.
Towards targeted prevention?
Although this discovery is still recent, it opens interesting perspectives for the prevention and detection of colorectal cancer in young people. The identification of colibactin as a potential risk factor could make it possible to develop new strategies to prevent the appearance of these cancers at an early age.
First of all, the detection of strains of E. coli producing colibactin could become a new early diagnosis tool. Indeed, a test to detect this toxin in the stool or intestine could help identify people at risk earlier, before the first symptoms appear.
Then, it would be possible to explore approaches to modify the intestinal microbiota of people at risk, using probiotics or specific antimicrobial treatments to eliminate pathogenic strains of E. coli producing colibactin. Another interesting avenue would be the use of treatments intended to inhibit the action of colibactin, so as to limit its mutagenic impact.
Finally, colorectal cancer screening recommendations could be revised to include earlier examinations, particularly for young adults with risk factors. Currently, systematic screening generally only begins at age 50. If colibactin is indeed a risk factor, it would be appropriate to lower this age limit.
A silent revolution in cancer research
This discovery represents a turning point in understanding the causes of the increase in early colorectal cancers. It invites us to rethink how the gut microbiota can affect our long-term health, and in particular to think about its role in triggering early cancers.
Although the research is still at a preliminary stage, highlighting the possible role of colibactin offers promising avenues for future research and treatments. It could also transform colorectal cancer prevention strategies, allowing us to identify risks in childhood, not in adulthood.
As one of the study’s lead researchers points out:
“We knew colorectal cancer was increasing among young people, but we didn’t know why. Now we have a lead. »
It is therefore possible that, in the near future, this avenue will lead to concrete solutions, making it possible to curb this silent epidemic.
