Scientists Discover a Cellular Switch That Could Help Prevent Stomach Cancer

Helicobacter pylori is one of the world’s most common bacterial infections, yet most people who carry it never develop symptoms. The troubling part? The same bacterium is a major cause of stomach cancer. Because it spreads mainly within families, the question of who faces the greatest risk can become deeply personal.

Now, researchers in Berlin have uncovered a possible explanation for how the infection triggers cancer-related changes.

Their discovery centers on a chain of signals connecting immune cells, connective tissue, and the stomach lining. When inflammation persists, those signals can push stomach cells into an unusual repair state that may become permanent.

Published in Nature Communications in September, the findings could eventually help doctors identify dangerous tissue changes before cancer develops.

No new treatment exists yet, and the experiments used animals and laboratory-grown tissue rather than patient trials. Still, the discovery raises an important question: what happens when the infection disappears but the damage remains?

The Tissue Beneath the Lining Turns Out to Be the Switch

Connective tissue does more than support the stomach lining.

Scientists already knew H. pylori could cause stomach cancer. What remained unclear was how inflammation produced lasting changes. The Berlin team’s study revealed something unusual: infected tissue grew rapidly, but its usual stem cells didn’t multiply accordingly.

Researchers traced the changes to disrupted BMP signaling, which normally helps regulate renewal of the stomach lining.

Immune cells then released an inflammatory messenger called interleukin-1β, prompting connective tissue to activate a healing response.

That response pushed stomach cells into a repair program normally associated with embryonic development and wound healing. With persistent inflammation, however, the program continued, driving cell division and long-term remodeling.

First author Giulia Beccaceci explained to Max Delbrück Center: “So connective tissue isn’t just a bystander, but the actual switch.”

Five Ways of Looking at the Same Tissue

Each method answered a different piece of the question.

Researchers used single-cell sequencing to examine gene activity across tens of thousands of infected cells. Animal models with selective gene inactivation then helped establish which signals controlled the changes.

They also studied organoids, simplified stomach tissue grown in laboratories, and assembloids combining stomach lining with connective tissue. These experiments revealed that interleukin-1β prompted connective tissue to produce prostaglandin E2, activating a protein called YAP in the lining.

Publicly available human datasets helped researchers check whether similar cellular patterns occurred in people.

Related:10 Simple Habits to Recharge Your Mind and Body

Clearing the Infection Doesn’t Always Reset the Stomach

Testing and antibiotic treatment remain established ways to reduce stomach cancer risk.

Berlin laboratory leader Michael Sigal recommends testing for people with a family history of stomach cancer, symptoms, or a known infection.

A Nature Medicine trial followed 180,284 people across 980 villages in China for 11.8 years, recording 1,035 stomach cancers. Cancer occurrence was approximately 14% lower among those offered treatment and 19% lower among those whose infection was successfully cleared.

Yet eliminating the bacterium doesn’t always reverse the damage. Some stomach tissue may already be permanently reprogrammed, leaving an elevated cancer risk even after treatment.

Most Infections Never Turn Into Cancer

So the real prize is a way to spot the ones that might.

Duke researcher Meira Epplein estimated in 2022 that half the world’s population and one-third of Americans carry H. pylori. Yet approximately 3% of infected people develop cancer.

Sigal’s team is developing markers to identify those at higher risk.

“In order to reliably identify these individuals, we are currently developing markers that can detect, in mucosal tissue samples, whether the tissue is on its way to becoming precancerous,” he said to the Max Delbrück Center.

No markers or clinical timeline have been announced.

What the Researchers Are Building Next

The near-term plan is watching patients closely, with drugs further off.

Charité is establishing a Cancer Prevention Clinic to monitor people at elevated risk for stomach cancer. Tissue samples could help researchers identify changes that precede cancer.

Meanwhile, one potential drug strategy involves preventing connective tissue from responding to interleukin-1β.

Earlier population studies also associated certain anti-inflammatory medications with lower gastrointestinal tumor risk.

Those medications inhibit COX-2, an enzyme involved in this pathway, but the association does not prove they prevent stomach cancer. The most difficult question concerns tissue that has already changed.

Has anyone in your family ever been tested for H. pylori, and what led to the test?

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