H. pylori: A Silent Threat to Gastric Cancer

Authored By: Hanni Yang

Art By: Sophia Li Helicobacter pylori, or H. pylori for short, is a common stomach bacteria that primarily causes gastric cancer, one of the deadliest cancers in the world. If this bacterium infects the stomach lining, it can cause damage and inflammation that can eventually become a cancer [1]. Helicobacter pylori can be eliminated by antibiotics, but because of reinfection, drug resistance, and inadequate screening, gastric cancer incidence is still high. This article will discuss some possible causes of stomach cancer due to H. pylori, preventive and treatment strategies, and recent findings that may enhance cancer prevention. Establishing the correlation between H. pylori infection and stomach cancer would improve public health initiatives and reduce the rate of incidence of stomach cancer.

One of the main ways by which H. pylori induces cancer is chronic inflammation. When the bacteria infects the stomach, the immune system is provoked and starts degrading the gastric mucosa—the stomach lining protective layer. When the stomach lining is inflamed, the chance of genetic mutations that would make the normal cells develop into cancer cells will be increased. H.pylori also releases the virulence factor CagA, a protein that causes cellular dysfunction and uncontrolled cell growth [2]. According to a cancer research study led by Amin Talebi Bezmin Abadi and other researchers, people infected with H. pylori strains carrying the CagA (cytotoxin-associated gene A) gene are more likely to develop stomach cancer than people infected with CagA-negative H. pylori strains [3]. The CagA gene creates harmful proteins and makes it enter people’s stomach systems, disrupt their body, and increase the likelihood of developing cancer. CagA-positive H. pylori strains are having high incidences of stomach cancer in East Asian countries. These strains are more virulent than those in the West. On the other hand, CagA-negative strains are less damaging and less likely to cause cancer.

In addition to being inflammatory, H. pylori also changes genes and epigenetics, which also leads to cancer. Through DNA methylation, a chemical process where a chemical label is added to DNA and quiets the important genes, the infection can repress tumor suppressor genes, so that they cannot regulate abnormal cell growth. Furthermore, H. pylori changes the microbiota, a group of microorganisms that live in a specific body structure, of the stomach. This modification of microbiota throws off the regular balance of healthy flora and creates an environment that is conducive to the development of cancer [4]. The results indicate that H. pylori plays an important role in the development of stomach cancer.

Helicobacter pylori, despite carrying high risks of stomach cancer development from an untreated infection, is typically successfully treated. Eradication treatment, the most common treatment, is a combination of antibiotics and proton pump inhibitors to kill the infection and inhibit stomach acid to allow the healing of the stomach lining. According to a H. pylori study led by David Y Graham, H. pylori treatment could reduce the risk of stomach cancer by a significant amount, especially for those receiving therapy before precancerous changes develop [5]. However, the therapy no longer functions so effectively because certain forms of H. pylori resist antibiotics better. This is an ongoing problem revealing the need for other therapies as well as emerging treatments. Among the treatments is phage therapy, which uses viruses to infect and eliminate H. pylori bacteria. Unlike antibiotics, phage therapy does not destroy beneficial gut bacteria and has the potential to reduce the likelihood of resistance [6]. While this treatment is still in its research phase, it does promise much to reduce the risk of developing stomach cancer. It is a novel strategy that could one day revolutionize the way we fight recurrent infections like H. pylori in the future.

Preventive measures and treatments need to be implemented to reduce the occurence of H. pylori cancer. In high-risk regions like East Asia, large-scale screening programs prove to be effective in the cases before they become more serious [7]. Since H. pylori is most commonly spread through contaminated food, drinks, and human contact, improved sanitation and hygiene can help lower the rates of transmission. High rates of infection and long-term consequences can be avoided by improving awareness among the general public regarding the dangers of H. pylori and the need for early detection and prevention.

Despite the progress in treatment and prevention, there is still a high risk of getting gastric cancer. Eradication is not easy in the long-term because there is a chance of reinfection, especially in unsanitary conditions. Furthermore, most infected individuals are asymptomatic initially, and thus the cancer tends to go unnoticed until it is more developed. Because alterations in microbial diversity can influence how H. pylori interacts with the stomach lining, researchers continue to investigate the contribution of a person’s overall stomach microbiota to cancer formation [8].

In conclusion, H. pylori induces genetic damage, chronic inflammation, and disruption of the microbiome, which is a high risk for gastric cancer. Although infection rates have decreased as a result of antibiotic treatments and preventative initiatives, problems like drug resistance and reinfection still exist. Fighting this virus means ongoing expenditures on alternative therapies and public health programs. Treatment of H. pylori infections early on can improve global health outcomes and substantially reduce the risk of stomach cancer.

References

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Baj, J., Forma, A., Sitarz, M., Portincasa, P., Garruti, G., Krasowska, D., & Maciejewski, R. (2020, December 25). Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment. Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment. Retrieved March 9, 2025, from https://pmc.ncbi.nlm.nih.gov/articles/PMC7824444/

Bezmin Abadi, A. T., Rafiel, A., Ajami, A., Hosseini, V., Taghvaei, T., Jones, K. R., & Merrell, D. S. (2011, September 1). Helicobacter pylori homB, but Not cagA, Is Associated with Gastric Cancer in Iran▿,†. Helicobacter pylori homB, but Not cagA, Is Associated with Gastric Cancer in Iran▿,†. Retrieved March 9, 2025, from https://pmc.ncbi.nlm.nih.gov/articles/PMC3165595/

Valenzuela, M. A., Canales, J., Corvalan, A. H., & Quest, A. F. (2015, December 7). Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis. Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis. Retrieved March 9, 2025, from https://pmc.ncbi.nlm.nih.gov/articles/PMC4671030/

Graham, D. Y. (2015, February 2). Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits. Helicobacter pylori Update: Gastric Cancer, Reliable Therapy, and Possible Benefits. Retrieved March 9, 2025, from https://pmc.ncbi.nlm.nih.gov/articles/PMC4375058/

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