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      Potential antigen candidates for subunit vaccine development against Helicobacter pylori infection

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          Pathobiology of Helicobacter pylori-Induced Gastric Cancer.

          Colonization of the human stomach by Helicobacter pylori and its role in causing gastric cancer is one of the richest examples of a complex relationship among human cells, microbes, and their environment. It is also a puzzle of enormous medical importance given the incidence and lethality of gastric cancer worldwide. We review recent findings that have changed how we view these relationships and affected the direction of gastric cancer research. For example, recent data have indicated that subtle mismatches between host and microbe genetic traits greatly affect the risk of gastric cancer. The ability of H pylori and its oncoprotein CagA to reprogram epithelial cells and activate properties of stemness show the sophisticated relationship between H pylori and progenitor cells in the gastric mucosa. The observation that cell-associated H pylori can colonize the gastric glands and directly affect precursor and stem cells supports these observations. The ability to mimic these interactions in human gastric organoid cultures as well as animal models will allow investigators to more fully unravel the extent of H pylori control on the renewing gastric epithelium. Finally, our realization that external environmental factors, such as dietary components and essential micronutrients, as well as the gastrointestinal microbiota, can change the balance between H pylori's activity as a commensal or a pathogen has provided direction to studies aimed at defining the full carcinogenic potential of this organism.
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            Global burden of cancers attributable to infections in 2008: a review and synthetic analysis.

            Infections with certain viruses, bacteria, and parasites have been identified as strong risk factors for specific cancers. An update of their respective contribution to the global burden of cancer is warranted. We considered infectious agents classified as carcinogenic to humans by the International Agency for Research on Cancer. We calculated their population attributable fraction worldwide and in eight geographical regions, using statistics on estimated cancer incidence in 2008. When associations were very strong, calculations were based on the prevalence of infection in cancer cases rather than in the general population. Estimates of infection prevalence and relative risk were extracted from published data. Of the 12·7 million new cancer cases that occurred in 2008, the population attributable fraction (PAF) for infectious agents was 16·1%, meaning that around 2 million new cancer cases were attributable to infections. This fraction was higher in less developed countries (22·9%) than in more developed countries (7·4%), and varied from 3·3% in Australia and New Zealand to 32·7% in sub-Saharan Africa. Helicobacter pylori, hepatitis B and C viruses, and human papillomaviruses were responsible for 1·9 million cases, mainly gastric, liver, and cervix uteri cancers. In women, cervix uteri cancer accounted for about half of the infection-related burden of cancer; in men, liver and gastric cancers accounted for more than 80%. Around 30% of infection-attributable cases occur in people younger than 50 years. Around 2 million cancer cases each year are caused by infectious agents. Application of existing public health methods for infection prevention, such as vaccination, safer injection practice, or antimicrobial treatments, could have a substantial effect on the future burden of cancer worldwide. Fondation Innovations en Infectiologie (FINOVI) and the Bill & Melinda Gates Foundation (BMGF). Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Oncogenic mechanisms of the Helicobacter pylori CagA protein.

              Infection with strains of Helicobacter pylori that carry the cytotoxin-associated antigen A (cagA) gene is associated with gastric carcinoma. Recent studies have shed light on the mechanism through which the cagA gene product, CagA, elicits pathophysiological actions. CagA is delivered into gastric epithelial cells by the bacterial type IV secretion system, where it deregulates the SHP2 oncoprotein. Intriguingly, CagA is noted for its variation, particularly at the SHP2-binding site, which could affect the potential of different strains of H. pylori to promote gastric carcinogenesis.
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                Author and article information

                Contributors
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                Journal
                Journal of Cellular Physiology
                J Cell Physiol
                Wiley
                0021-9541
                1097-4652
                December 2019
                June 12 2019
                December 2019
                : 234
                : 12
                : 21460-21470
                Affiliations
                [1 ]Antimicrobial Resistance Research Center, Bu‐Ali Research Institute Mashhad University of Medical Sciences Mashhad Iran
                [2 ]Department of Microbiology and Virology, School of Medicine Mashhad University of Medical Sciences Mashhad Iran
                [3 ]Cancer Research Center Semnan University of Medical Sciences Semnan Iran
                [4 ]Department of Immunology Semnan University of Medical Sciences Semnan Iran
                [5 ]Department of Biology, Tehran Central Branch Islamic Azad University Tehran Iran
                [6 ]Department of Microbiology and Virology, School of Medicine Jiroft University of Medical Sciences Jiroft Iran
                Article
                10.1002/jcp.28870
                31188484
                09250aa2-789e-4984-bce0-bb0aa7c81be5
                © 2019

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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