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SCIENCE NEWS

Stomach Cancer: Helicobacter Is Not the Only Culprit

  • Writer: Jenner Nex
    Jenner Nex
  • 2 days ago
  • 3 min read

The Oral Bacterium Streptococcus anginosus Also Promotes Stomach Cancer


Microbes as Cancer Triggers: It is well known that Helicobacter pylori can cause stomach cancer. But there is another culprit: The bacterium Streptococcus anginosus also promotes the growth of cancerous tumors in the stomach, as a new study has confirmed. According to the study, this microbe is not only found in increased numbers in stomach cancer ulcers, but it also releases methionine, a molecule that facilitates the energy supply of cancerous tumors and promotes their growth.

Stomach cancer is the fifth most common cancer worldwide. Until now, the primary triggers for these adenocinomas of the stomach lining were considered to be diet, genetic factors, and the stomach bacterium Helicobacter pylori. This bacterium causes chronic inflammation of the stomach lining and promotes the development of cancerous tumors. However, several other bacteria are now also suspected of promoting stomach ulcers, including some microbes that live in the oral cavity.


A Second Suspect


Researchers led by Chengbei Zhou from Shanghai Jiao Tong University have now confirmed one of these suspects as the culprit: the bacterium Streptococcus anginosus. This chain-forming, spherical microbe is primarily found in our mouth and throat, where it is usually harmless. However, the bacterium can also colonize the mucous membranes of the respiratory tract and the digestive tract. In immunocompromised individuals, it can cause inflammation—this much is known.


But for some time now, Streptococcus anginosus has also been suspected of being involved in stomach cancer. In 2022, it was shown that stomach cancer patients often have elevated levels of this bacterium in their stool. Zhou and her colleagues followed up on this lead. For their study, they examined stomach cancer tumors for Streptococcus anginosus, isolated the bacteria, and investigated in cell cultures and animal experiments whether and how the germs influence tumor growth.


Oral Bacteria, Methionine, and Stomach Tumors


The team discovered three different strains of Streptococcus anginosus in the tumors of stomach cancer patients. The bacteria were also found in increased numbers in their gastric microbiome. Further analysis revealed that these microbes produce and release particularly high levels of methionine. This sulfur-containing amino acid is essential for our metabolism.


"Previous studies have also shown that methionine can accelerate the growth of cancerous tumors," the researchers explain. To investigate the role of Streptococcus anginosus in this process, they infected cancer cell cultures and mice with stomach cancer with the bacteria. The results showed that "methionine enhances the expression of the enzyme MAT2A and its transport into cells," the researchers write. "This provides the tumor cells with energy and promotes their growth."


This was also confirmed in tests with mice: The animals' stomach cancer tumors grew faster when Streptococcus anginosus was present in their gut flora, the team reports. However, this only applied if the bacteria were actually able to produce methionine. If this production was blocked in the microbes, the cancer-promoting effect was absent.


Streptococcus anginosus confirmed as a risk factor


This makes it clear that, in addition to the stomach bacterium Helicobacter pylori, the oral bacterium Streptococcus anginosus can also increase the risk of stomach cancer and promote the growth of stomach ulcers. "Our results shed light on the complex metabolic interaction between Streptococcus anginosus and its host," write Zhou and her colleagues.


"The results also highlight the important role of methionine produced by these bacteria in the progression of stomach cancer," the team continues. The new findings could help to identify an increased risk of stomach cancer early on using stool samples. At the same time, they offer a potential approach for prevention and therapy. (Gut, 2025; doi: 10.1136/gutjnl-2025-336966)


Source: BGI Genomics

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