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Exposure to toxin increases colorectal cancer risk among younger adults, study finds

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Exposure to toxin increases colorectal cancer risk among younger adults, study finds

Amid the alarming trend of colorectal cancer cases rising among young people, a new study has pinpointed a potential source.

Researchers from University of California San Diego have linked a bacterial toxin called colibactin to the increase in early-onset cases.

Colibactin is produced by certain strains of Escherichia coli (E. coli) that exist in the colon and rectum, according to the researchers.

COLORECTAL CANCER RISK REDUCED BY THIS COMMON VITAMIN, STUDY SUGGESTS

Exposure to the bacterial toxin during early childhood can alter the DNA of colon cells in a way that increases the risk of developing colorectal cancer before age 50, the study found.

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In the study, the researchers analyzed 981 colorectal cancer genomes from early-onset and late-onset colorectal cancer patients across 11 countries.  (iStock)

The study, which was funded by Cancer Research UK, was published in the journal Nature on April 23.

“The key takeaway is that exposure to colibactin is likely a major contributor to early-onset colorectal cancer,” senior author Ludmil Alexandrov, professor in the Shu Chien-Gene Lay Department of Bioengineering and the Department of Cellular and Molecular Medicine at UC San Diego, told Fox News Digital.

“They could be decades ahead of schedule for developing colorectal cancer.”

In the study, the researchers analyzed 981 colorectal cancer genomes from early-onset and late-onset colorectal cancer patients across 11 countries. 

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Those who had prior exposure to colibactin were found to have specific mutations in their DNA, which have been shown to mainly occur in the first decade of life — “placing children on an accelerated path to developing cancer as young adults.”

Exposure to the bacterial toxin during early childhood can alter the DNA of colon cells in a way that increases the risk of developing colorectal cancer before age 50, the study found. (iStock)

That group was 3.3 times more likely to develop early-onset colorectal cancer compared to those who were diagnosed after 70.

These mutations were found to make up 15% of the early genetic alterations that increase colorectal cancer risk.

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“We detected the mutational signature of colibactin in over 50% of colorectal tumors from patients under 40, compared to less than 10% in tumors from older individuals,” Alexandrov noted.

“If someone acquires one of these driver mutations by the time they’re 10 years old, they could be decades ahead of schedule for developing colorectal cancer, getting it at age 40 instead of 60,” noted Alexandrov.

The fact that a microbial exposure in the first few years of life can leave a “lasting genomic imprint” and likely contribute to cancer in adulthood is both “remarkable and sobering,” according to the researcher. 

“It’s a reminder that there are likely many other such exposures we’ve yet to uncover, and that the way we nurture and protect children during these formative years may have long-term implications for their lifelong health,” he told Fox News Digital. 

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“From my perspective, investing in early-life prevention, healthy living and research is not just important — it’s essential.”

Dr. Emil Lou, MD, PhD, a board-certified oncologist and internal medicine physician at the University of Minnesota, agrees that the microbiome – “the constellation of microbes that includes bacteria that live under normal circumstances in our gut” — is one potential culprit of early-onset colorectal cancer.

“It is less surprising now than it was a decade ago that any form of bacteria – more specifically, a toxin derived from bacteria – could be associated with and potentially be the primary cause of cancer,” Lou, who was not involved in the study, told Fox News Digital. 

“What is especially concerning is the long period of time that might lapse between exposure to the bacteria early in life, and the time before the related cancer is diagnosed.”

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Potential limitations

Alexandrov pointed out that the study provides “strong genomic evidence” of a “striking association” between colibactin and early-onset colorectal cancer, but cannot prove causation. 

“Demonstrating unequivocal causality — proving that colibactin alone is sufficient to initiate cancer in humans — remains a significant challenge,” he told Fox News Digital.

Colorectal cancer cases have doubled among adults under 50 for each of the past two decades, statistics show. (iStock)

“Definitive proof of causality would require long-term prospective studies beginning in early childhood to monitor microbial colonization and track cancer development over several decades.”

Lou agreed with this limitation, noting the complexity of cancer factors.

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“There are many aspects of our environment – both within and outside of our bodies – that can play a role in development of cancer,” he said. “It is difficult to say or conclude whether any given single factor – in this case, the bacteria-derived toxin – is the true or even a major cause of colorectal cancer.”

“Providing evidence of potential association sets the foundation for more in-depth studies to determine whether there is true cause and effect,” Lou added.

“If current trends continue, colorectal cancer is projected to become the leading cause of cancer-related death among young adults by 2030.”

Alexandrov noted that while the findings don’t yet warrant changes to screening or treatment guidelines, they do highlight the “critical role of early-life microbial exposures” in terms of long-term cancer risk. 

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“We are actively working on developing screening tests to detect the long-term effects of colibactin exposure, with the goal of translating these findings into practical prevention strategies in the near future,” he added.

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Colorectal cancer cases have doubled among adults under 50 for each of the past two decades, statistics show.

“If current trends continue, colorectal cancer is projected to become the leading cause of cancer-related death among young adults by 2030,” the researchers concluded.

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New ways to prevent flu revealed in ‘accidental’ lab breakthrough, study finds

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New ways to prevent flu revealed in ‘accidental’ lab breakthrough, study finds

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An accidental lab discovery has opened the door to entirely new ways of preventing the flu.

While investigating how influenza replicates, researchers discovered that different flu strains use completely different strategies to infiltrate human cells, SWNS reported.

By targeting the specific molecules the viruses rely on, scientists found that they could block them from entering new cells and halt their replication altogether.

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Researchers say these “fundamental insights” into seasonal influenza highlight a clear path toward developing better preventive medications.

“The hope is that fundamental, curiosity-based research like this helps to pave the way for novel strategies to treat and prevent influenza infections,” principal investigator Dr. Emily Bruce, from the University of Vermont’s Larner College of Medicine, said in the SWNS report.

While investigating how influenza replicates, researchers discovered that different flu strains use completely different strategies to infiltrate human cells. (iStock)

While several flu strains cause illness, H1N1 and H3N2 influenza A viruses are the most common. However, current flu tests cannot differentiate between them, and clinical treatments are identical for both.

Although vaccines and antivirals are available, Bruce noted a “dire” need for better medications to stop the virus from spreading cell to xxcell.

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“You don’t get sick when a virus is in one cell,” he noted. “You get sick because a virus replicates itself and goes into many more cells.”

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The study, which was published in The Journal of Virology, originally aimed to map how viral RNA segments are transported within cells to create new viral particles.

The team used H1N1 and H3N2 viruses isolated from the nasal passages of positive patients in 2022.

Clinical treatments remain identical for both primary strains of the flu virus. (iStock)

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During the investigation, the team unexpectedly stumbled upon a cellular pathway that blocked the virus from entering lung cells, SWNS reported.

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The data revealed that when a specific human protein called Rab11B was depleted, H3N2 viruses failed to enter human lung cells. H1N1 viruses were completely unaffected.

Using reverse genetics, the team mapped this defect and uncovered a brand-new, H3N2-specific role for Rab11B during viral entry.

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This discovery challenged the scientific assumption that all flu viruses enter cells the same way.

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“Viruses are like pirates from different countries hijacking someone’s ship,” Bruce said. “Different viruses, like different types of pirates, use different methods to get onboard.”

This discovery challenged the scientific assumption that all flu viruses enter cells the same way. (iStock)

“We had previously thought that all flu viruses used the same way to get into a cell, but we discovered that this is not true,” she went on. “H1N1 and H3N2 need different proteins to get in, and if you get rid of the right protein, a specific virus can’t get in.”

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While these findings identify a critical cellular pathway for viral entry, the study was conducted using isolated cells, the researchers acknowledged.

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Further research is needed to determine whether blocking the protein is safe and effective within a live, complex human respiratory system.

Bruce and the team hope to conduct further research to determine whether this Rab11B-dependency is a fundamental property of H3N2, or if it’s a trait unique to currently circulating flu strains.

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One extra serving of processed meat a day linked to higher cancer risk

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One extra serving of processed meat a day linked to higher cancer risk

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Eating processed meat like ham, sausage and bacon may be linked to a higher risk of certain types of cancer, according to new research.

While health organizations have already confirmed that processed meat can contribute to colon cancer, this study looked closer at cancers in the upper digestive tract, where the link has historically been less clear.

To understand these connections, researchers from the European Prospective Investigation into Cancer and Nutrition (EPIC), one of the world’s largest long-term nutrition and cancer cohorts, tracked the health and diets of 450,112 people across Europe for an average of 14 years. 

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The study group included 131,426 men and 318,686 women, according to the study’s press release.

During the follow-up period, 876 people developed stomach cancer and 215 people developed esophageal adenocarcinoma, which is cancer of the tube connecting the mouth to the stomach.

For female participants, eating both processed meat and white meat was linked to an increased risk of developing the disease. (iStock)

Researchers tracked where the stomach cancers grew, separating them into the upper part of the stomach near the throat and the lower part of the stomach.

The researchers also sorted the tumors into two categories based on how the cancer cells appeared under a microscope: intestinal, which forms more organized structures, and diffuse, in which the cells are more scattered throughout the tissue.

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After adjusting for other lifestyle factors, the researchers found that for every extra 30 grams of processed meat a person ate per day, their overall risk of stomach cancer went up by 9%. Eating that same extra 30 grams a day was also linked to a 13% higher risk of esophageal adenocarcinoma.

A standard single slice of regular deli-sliced ham or lunch meat averages around 28 grams, according to USDA data and nutritional tracking databases.

An extra 20 grams of white meat, such as chicken and turkey, was linked to a 12% higher risk of cancer in the main body of the stomach. (iStock)

An extra 20 grams of white meat, such as chicken or turkey, was linked to a 12% higher risk of cancer in the main body of the stomach, the researchers noted.

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The study also revealed differences between men and women. For male participants, only processed meat showed a clear, statistically significant link to a higher risk of stomach cancer. For female participants, however, eating both processed meat and white meat was linked to an increased risk.

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These findings align with global health benchmarks, particularly those established by the World Health Organization’s International Agency for Research on Cancer.

The agency has long classified processed meat as a known human carcinogen, primarily due to its strong, well-documented links to colorectal cancer.

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However, health organizations have also consistently pointed to a potential, yet less definitive, relationship between these meats and cancers of the stomach.

Eating 30 grams of processed meat a day, or the equivalent to one slice of ham, was linked to a 13% higher risk of esophageal adenocarcinoma. (iStock)

Further scientific investigation is needed to confirm the findings and to account for other underlying risk factors, such as certain stomach infections, which could interact with dietary habits.

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A key limitation of the study is its reliance on self-reported diets, which can sometimes lead to inaccuracies in how participants recall their meat consumption over time, the researchers noted.

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The findings were published in the International Journal of Cancer.

Fox News Digital reached out to the researchers requesting comment.

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The Surprising Hormone That Could Make Menopause Weight Loss Easier

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The Surprising Hormone That Could Make Menopause Weight Loss Easier


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The Hormone That Could Make Menopause Weight Loss Easier




















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