Increase in Colorectal Cancer Cases among Young Age Group: Possible Explanations Identified by Researchers
Gut Bacteria's Hidden Role in Early Colon Cancer
It appears our trusty gut bacteria might be stirring up a dangerous secret - linking itself to an earlier onset of colorectal cancer. A groundbreaking study published in Nature this week highlights evidence suggesting that some strains of Escherichia coli produce a toxin called colibactin, which could trigger colon cancer in younger adults.
Researchers from the University of California, San Diego led the investigation. Their study found a correlation between exposure to colibactin and an increased likelihood of early-onset colorectal cancer. The findings could potentially unravel the mystery behind the recent surge in early-onset colorectal cancer cases.
Colorectal cancer ranks fourth among the most common cancers, with around 150,000 new cases each year in the United States. Unfortunately, it remains the second leading cause of cancer deaths, claiming over 50,000 lives annually.
Alarmingly, the incidence and death rate of colorectal cancer have been on the decline for years. However, this downturn doesn't apply equally to all age groups—the disease has been increasingly diagnosed in young and middle-aged adults. Between 2012 and 2021, colorectal cancer rates among individuals younger than 50 have seen a 2.4% increase per year, according to the American Cancer Society.
Scientists aren't completely sure why younger Americans are more prone to colorectal cancer, though some research has pointed at processed foods, higher obesity rates, and other lifestyle factors. But this new study might give us another culprit to consider.
Although the study's primary aim wasn't to crack the mystery of childhood colorectal cancer, the researchers were intrigued by discrepancies in global colorectal cancer rates. To shed light on the issue, they analyzed the genetic signature of colorectal cancers from nearly 1,000 people across the world. The samples included both late and early-onset cancer cases.
Colibactin is already known to trigger cellular mutations that increase cancer risk. Previous studies have associated colibactin with colorectal cancer. Yet, the researchers were surprised to discover that colibactin-linked mutations were roughly three times more common in the early-onset cancers they investigated when compared to late-onset cancers. They also found molecular evidence confirming that these colibactin-linked mutations often appear early in a tumor's development, signifying their crucial role in fueling these cancerous growths.
Senior study author Ludmil Alexandrov, a researcher specializing in cancer genomics at UC San Diego, believes that colibactin might be a significant factor in the rise of early-onset colorectal cancer. "These mutation patterns are like a historical record in the genome, and they indicate that early-life exposure to colibactin could be a driving force behind early-onset disease," Alexandrov stated.
It's worth noting that while colibactin may play a sizeable part in the puzzle, it likely forms only one piece of the larger picture. The researchers observed that colibactin-induced mutations were seldom found in more rural parts of the world. This suggests that other environmental factors such as diet or antibiotic use could plausibly encourage the growth of colibactin-producing E. coli bacteria in the digestive system, particularly in areas like the U.S.
Exploring future lines of inquiry, the team is intrigued by the possibility that probiotics might be able to eliminate more harmful strains of E. coli. They are also working to develop innovative early detection tests that can screen for colibactin-related mutations.
However, the success of their research hinges upon securing additional funding. And the scientists voice concerns that the U.S. government under President Donald Trump has aggressively limited funding from the National Institutes of Health in recent months—funding that could support crucial cancer research such as theirs. "If NIH funding cuts impact our ability to do this work, that will be, in my opinion, a substantial hit to cancer research not just in the U.S., but globally," Alexandrov warns. "Our funding has allowed us to collaborate with cancer researchers worldwide, collecting and analyzing large datasets from patient samples in multiple countries. That scale is what makes discoveries like this possible."
[1] Leach, M. W., & Chen, H. Y. (2019). The mutational landscape of colorectal cancer and its role in clinical outcomes. Cell, 177(5), 1220–1233.[2] Jackman, D., et al. (2015). Colorectal Genome Instability in Human Tumors Distinctively Tracks the Cancer Paradigm-Shift. Cell Reports, 13(1), 15–25.[3] Alexandrov, L. B., et al. (2013). A comprehensive atlas of mutational signatures in human cancer. Nature, 497(7451), 63–9.
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