The Australian scientists Barry Marshall and Robin Warren discovered Helicobacter pylori in 1982. It is a Gram-negative spiral bacterium. Infection often occurs in childhood. The World Health Organization (WHO) declared Helicobacter pylori a Class I carcinogen because it plays a primary role in gastric cancer development.
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Association between Helicobacter Pylori and Gastric Cancer
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The bacterium Helicobacter pylori primarily causes gastric adenocarcinoma and shows a strong link to distal gastric cancer.
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It also has a clear causal relationship with gastric MALT lymphoma.
Fig 1. Pathogenesis of Helicobacter pylori and its effects on cells (Elbehiry, A., et al. 2023).
Mechanism of Helicobacter Pylori Carcinogenesis
Helicobacter pylori (HP) is a bacterium that colonizes the stomach and has been identified as an important cause of human gastric cancer (especially gastric adenocarcinoma) and related gastric diseases (such as gastritis and gastric ulcers). Its carcinogenic mechanism mainly includes the following aspects:
- Chronic inflammation: Helicobacter pylori infection can cause chronic gastritis. Long-term inflammatory response leads to damage and regeneration of epithelial cells, increasing the risk of carcinogenesis.
- Apoptosis and proliferation: Toxins released by Helicobacter pylori can interfere with the signal transduction pathways of host cells, promote cell proliferation, and inhibit cell apoptosis, thereby providing favorable conditions for carcinogenesis.
- Gene mutation: Helicobacter pylori infection can cause DNA damage and stimulate gene mutations, especially in genes related to cell cycle regulation and apoptosis.
- Immune response: After infection with Helicobacter pylori, the body will produce an immune response, which may lead to the immune system's attack on normal cells, aggravating tissue damage and possibly promoting the development of cancer.
- Microenvironment changes: The presence of Helicobacter pylori will change the gastric microenvironment, such as changes in pH value and the composition of bacterial communities, which may contribute to the formation of cancer.
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Producing carcinogens: Helicobacter pylori can metabolize certain substances to produce carcinogens, which may directly damage cells and cause cancer.
These mechanisms can interact with each other to form a complex carcinogenic process. Understanding these mechanisms will help develop treatments for Helicobacter pylori, as well as early cancer screening and prevention strategies.
Molecular Mechanism
| Mechanisms |
Description |
| VacA toxin |
Induce cell apoptosis and immune escape |
| Oxidative stress |
Cause DNA damage and mutation |
| Chronic inflammation |
Inflammatory factors (such as IL-1β, TNF-α) promote the development of cancer |
Association between Helicobacter pylori and gastric cancer
Helicobacter pylori is a Gram-negative bacterium that is widely present in the human stomach. Several studies have shown that there is a significant association between Helicobacter pylori infection and gastric cancer. Specifically, the following aspects outline this association:
Carcinogenicity
The World Health Organization (WHO) classifies Helicobacter pylori as a Class I carcinogen, indicating that it has clear carcinogenicity to humans. Long-term infection with Helicobacter pylori can cause chronic inflammation of the gastric mucosa, which then develops into gastritis, gastric ulcers, and may eventually lead to gastric cancer.
Mechanism
Chronic inflammation caused by Helicobacter pylori infection may promote carcinogenesis through multiple mechanisms, including inducing cell proliferation, causing DNA damage, and changing immune responses. In addition, some strains of Helicobacter pylori may be more carcinogenic. These strains can produce specific toxins that promote the malignant transformation of cells.
Epidemiological Studies
Many epidemiological studies have found that the incidence of gastric cancer in people infected with Helicobacter pylori is significantly higher than that in uninfected people.
Epidemiological Evidence
The risk of gastric cancer in people infected with Helicobacter pylori is 3 to 6 times higher than that in uninfected people.
Helicobacter Pylori Eradication and Gastric Cancer Prevention
- Eradication therapy (standard triple or quadruple therapy)
- Antibiotics (such as clarithromycin, amoxicillin)
- Proton pump inhibitors (PPI)
- Bismuth
Prevention Strategies
- Survey of populations in high-incidence areas
- Focus on intervention for those with family history or precancerous lesions
- Regular gastroscopy follow-up after eradication
Helicobacter Pylori is Closely Related to Hastric Cancer
The application of antibiotic combination therapy for Helicobacter pylori eradication demonstrates effectiveness in lowering gastric cancer risk. The systematic detection and treatment of Helicobacter pylori infections could serve as a valid method to decrease gastric cancer rates. Healthcare professionals can best manage gastric cancer risk by controlling Helicobacter pylori infection. This infection leads to gastric mucosal malignancy via extended chronic inflammation and virulence factors which eventually results in gastric cancer.
Helicobacter pylori infection stands as a major risk element for gastric cancer development but genetic predispositions combined with dietary patterns and tobacco use equally contribute to cancer emergence.
The interplay between Helicobacter pylori infection and gastric cancer formation involves several mechanisms that create a complex and significant relationship. Implementing early screening along with eradication treatment holds substantial importance.
References
- Elbehiry, A., et al. Helicobacter pylori infection: current status and future prospects on diagnostic, therapeutic and control challenges. Antibiotics. 2023, 12(2): 191.
- Moss, S., et al. Evolving concepts in Helicobacter pylori management. Gastroenterology. 2024, 166(2): 267-283.
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