A new facet in our understanding of stomach cancer has emerged with the identification of Streptococcus anginosus as a significant player alongside the more notorious Helicobacter pylori. These findings have unlocked a potential dual threat within our own microbiome, revolutionizing the pathway towards innovative treatments.
The prevalence of H. pylori is widespread, colonizing the gut of roughly half the global population. While benign in most cases, its transformation into a pathogenic form presents a notable risk for stomach cancer, yet only a fraction of those infected actually develop the condition. This discrepancy has drawn researchers to hunt for additional culprits in the onset of the disease.
Joint efforts by scientists at Nanyang Technological University, Singapore, and the Chinese University of Hong Kong have brought to light the culpability of S. anginosus, typically part of the innocuous flora of the mouth and gut. Despite its general harmlessness, when the immune system is weakened, S. anginosus can transform into an opportunistic pathogen. The research findings were initially reported in the journal Cell and encapsulated the elaborate connection between this bacterium and gastric cancer progression.
Experiments on mouse models revealed that S. anginosus instigates a cascade of inflammatory responses, mirroring the early stages of human gastric cancer development. Significantly, the coinfection with H. pylori resulted in heightened gastric inflammation, indicating a probable synergistic effect in promoting gastritis, a precursor to cancer.
Joseph Sung Jao Yiu, co-corresponding author of the study and Emeritus Professor of Medicine at CUHK, accentuated the implications of their discovery: “The discovery of enrichment of S. anginosus in the gastric mucosa across different stages of cancer opens up a whole new direction in understanding the pathogenesis of gastric cancer.” Sung further underscored the heightened risk of gastric issues arising from the co-infection of the two bacteria.
Another facet of this groundbreaking study was the revelation of S. anginosus’s reliance on a specific surface protein, TMPC, to interact with the ANXA2 receptor on stomach lining cells, leading to the promotion of cancer progression. Curbing the activity of this receptor hindered the bacterium’s ability to trigger the MAPK enzyme pathway, a critical signal in cell proliferation and survival. Professor Yu Jun, from CUHK, spotlighted this discovery’s potential: “We have established the role of S. anginosus in gastric carcinogenesis and its related mechanism; next, we will explore the therapeutic potential of targeting it to reduce gastric inflammation and cancer risk.”
Beyond the laboratory, the implications of this research are profound. With gastric cancer ranking as the fifth most common malignancy globally, understanding the interplay between H. pylori and S. anginosus is essential. This could lead to innovative screening techniques, utilizing the detection of S. anginosus as a predictor for stomach cancer risk, possibly revolutionizing prevention strategies.
Moreover, the resilience of S. anginosus in acidic environments and its ability to survive in the stomach, even in the absence of H. pylori, elevates its significance in cancer research. Professor Sung advised that oral hygiene could be a simple yet effective measure to mitigate the risk of gastric cancer, a notion that further highlights the interconnectedness of our body’s ecosystems.
Relevant articles:
– A common, usually harmless bacteria (H. pylori) have a significant role in causing stomach cancer | Researchers identified the bacteria’s mechanism of action, opening the door to developing therapeutics to reduce the risk.
– Bacteria commonly found in the body contribute to stomach cancer, finds study, Medical Xpress, Mon, 18 Mar 2024 14:16:05 GMT
– New pathogen on the block, Nature.com, Mon, 11 Mar 2024 12:25:14 GMT
– ‘Significant discovery’: Hong Kong study identifies certain bacteria as risk factor for stomach cancer, South China Morning Post, Wed, 13 Mar 2024 12:33:18 GMT