How stomach cancer learns to grow on its own

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Stomach cancer is still one of the most common and deadly cancers in East Asia, especially in countries like Korea.

But even though it affects many people, scientists have not studied it as deeply as other cancers like colorectal cancer. Because of this, many of the ideas used to understand stomach cancer come from research on colon cancer—and don’t always work.

One mystery that has puzzled researchers for years is how stomach cancer even begins. In a healthy stomach, cells need signals from nearby cells to grow and survive. These signals come from what’s called the “microenvironment.”

If these support signals are missing, the cells usually stop growing. But cancer cells ignore this rule. They manage to grow without help. Until now, scientists didn’t know how stomach cancer cells managed to do this.

A new study led by Dr. Lee Ji-Hyun, Dr. Koo Bon-Kyoung, and Dr. Lee Heetak, working with researchers in Korea and Germany, has finally found the answer. The research was published in the journal Molecular Cancer and explains how early stomach cancer cells become independent and start growing on their own.

The key lies in two important cell signaling systems—WNT and MAPK. These are like instruction systems that tell cells when to grow or stop.

In healthy stomach cells, WNT signals are provided by nearby helper cells, allowing the stomach lining to stay balanced. If these signals disappear, the stomach cells can’t grow. But in early stomach cancer, something changes.

In colon cancer, mutations turn on the WNT signal permanently. But in stomach cancer, those same mutations are rare. So how do stomach cancer cells keep growing?

The new study found that early stomach cancer cells find a different solution. They start making their own WNT signals. Instead of waiting for help, the cancer cells begin “talking” to themselves. This change is triggered by another signal system called MAPK, which is often turned on in stomach cancer because of mutations in genes like KRAS or HER2.

Once MAPK is activated, it causes the cells to produce a special WNT molecule called WNT7B. This molecule creates a feedback loop—telling the same cell to keep growing, without needing outside signals.

This discovery is important because it shows how stomach cancer begins at the very earliest stage. The cancer cells become self-sufficient early, allowing them to grow unchecked.

To make sure the results were accurate, the scientists tested their findings in both mice and in lab-grown mini-tumors called organoids, made from real human cancer tissue.

These organoids mimic real tumors and confirmed the same behavior was happening in human patients. Samples were collected with the help of researchers from Yonsei University and a hospital in Germany.

The study also offers hope for better treatments. Right now, there are no good targeted drugs for this type of stomach cancer. But by finding out how these cancer cells fuel themselves, scientists now have new ideas for stopping the disease early—before it spreads or becomes more dangerous.

This work also shows a new direction in cancer research. Instead of only using animals to study disease, researchers are now using patient-derived models like organoids. These tools help make sure the science applies to real people.

This discovery not only solves a long-standing mystery about stomach cancer but may lead to better ways to treat and even prevent it in the future.

If you care about cancer, please read studies that artificial sweeteners are linked to higher cancer risk, and how drinking milk affects risks of heart disease and cancer.

For more health information, please see recent studies about the best time to take vitamins to prevent heart disease, and results showing vitamin D supplements strongly reduces cancer death.

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