Carcinogenesis and infection with Helicobacter pylori.
Gianina MicuFlorica StăniceanuSabina ZuracAlexandra BastianEliza GrămadaLuciana NichitaCristiana PoppLiana SticlaruR AndreiClaudiu Socoliuc
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Abstract:
It was accepted several years ago that, in the carcinogenesis process of human cancers, biologic agents, especially the viruses, are playing an etiologic role. This is the case of lymphomas (retroviruses), hepatocarcinoma (hepatic viruses) and cervical carcinoma (papilloma viruses). Helicobacter pylori is the first bacteria recognized as a first class carcinogen for gastric cancer. Nevertheless, comparing with the most validated human carcinogens, the activity of H. pylori is very little studied. As a consequence, at this moment, in its case, explanation of carcinogenesis mechanism is more or less hypothetical.Keywords:
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Gastric cancer (GC) is one of the most common carcino ma and the second leading cause of cancerrelated deaths worldwide.Helicobacter pylori (H.pylori ) infection causes a series of precancerous lesions like gastritis, atrophy, intestinal metaplasia and dysplasia, and is the strongest known risk factor for GC, as supported by epidemiological, preclinical and clinical studies.However, the mechanism of H. pylori developing gastric carcinoma has not been well defined.Among infected individuals, approximately 10% develop severe gastric lesions such as peptic ulcer disease, 1%3% progresses to GC.The outcomes of H. pylori infection are determined by bacterial virulence, genetic polymorphism of hosts as well as environmental factors.It is important to gain further understanding of the pathogenesis of H. pylori infection for developing more effective treatments for this common but deadly malignancy.The recent findings on the bacterial virulence factors, effects of H. pylori on epithelial cells, genetic polymorphism of both the bacterium and its host, and the environmental factors for GC are discussed with focus on the role of H. pylori in gastric carcinogenesis in this review.
Intestinal metaplasia
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Gastric cancer still is a major concern as the third most common cancer worldwide, despite declining rates of incidence in many Western countries. Helicobacter pylori(H. pylori) is the major cause of gastric carcinogenesis, and its infection insults gastric mucosa leading to theoccurrence of atrophic gastritis which progress to intestinal metaplasia, dysplasia, early gastric cancer, and advanced gastric cancer consequently. This review focuses on multiple factors including microbial virulence factors, host genetic factors, and environmental factors, which can heighten the chance of occurrence of gastric adenocarcinoma due to H. pylori infection. Bacterial virulence factors are key components in controlling the immune response associated with the induction of carcinogenesis, and cag A and vac A are the most well-known pathogenic factors. Host genetic polymorphisms contribute to regulating the inflammatory response to H. pylori and will become increasingly important with advancing techniques. Environmental factors such as high salt and smoking may also play a role in gastric carcinogenesis. It is important to understand the virulence factors, host genetic factors, and environmental factors interacting in the multistep process of gastric carcinogenesis. To conclude, prevention via H. pylori eradication and controlling environmental factors such as diet, smoking, and alcohol is an important strategy to avoid H. pylori-associated gastric carcinogenesis.
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Bacterial infections have, traditionally, not been considered major causes of human cancer. However, specific bacteria may be implicated in the carcinogenesis process via the induction of chronic inflammation and production of carcinogenic bacterial metabolites. H. pylori is the first bacterium accepted by the International Agency for Research on Cancer as a definite cause of gastric cancer in humans. This association is supported by epidemiological data and a series of research observations. It is envisaged that H. pylori establishes a lifelong inflammation resulting in increased cell proliferation, production of mutagenic free radicals and N-nitroso compounds and, finally, development of gastric carcinoma.
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It is well known that the Helicobacter pylori (H. pylori) infection is one of the major causes of gastric cancer development. It can be the remarkable point in cancer prevention strategies, if one-week antibiotic therapy for H. pylori prevents the gastric carcinogenesis. Since the WHO had classified H. pylori as the type I carcinogen for gastric cancer in 1994, academic efforts to investigate whether the treatment of H. pylori infection can prevent gastric carcinogenesis or not have made continuously, however, they have failed to make sufficient evidences despite 15 years of work. In gastric carcinogenesis, a variety of factors is involved. These include specific toxic factors of H. pylori. Subjects with specific genetic polymorphisms associated with gastric carcinogenesis are known to be at high risk for gastric cancer development and dietary environment such as high salt food and nitrogen compound also increase the risk of gastric cancer. H. pylori is involved in the transition from normal mucosa to chronic gastritis. Chronic atrophic gastritis can progress to intestinal metaplasia, dysplasia and finally to adenocarcinoma. And reversibility is lost after the progression to intestinal metaplasia and dysplasia. Therefore, H. pylori eradication dose not simply grantee the prevention of gastric carcinogenesis. We expect that the eradication of H. pylori before the stage of irreversible changes can do preventive effect. And further researches about virulent factors, genetic polymorphism, and other possible environmental conditions related to gastric carcinogenesis are crucial part in establishing preventive strategies for gastric cancer. (Korean J Med 75:503-507, 2008)
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