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      Helicobacter pylori associated factors in the development of gastric cancer with special reference to the early-onset subtype

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          Abstract

          Nowadays, gastric cancer is one of the most common neoplasms and the fourth cause of cancer-related death on the world. Regarding the age at the diagnosis it is divided into early-onset gastric carcinoma (45 years or younger) and conventional gastric cancer (older than 45). Gastric carcinomas are rarely observed in young population and rely mostly on genetic factors, therefore provide the unique model to study genetic and environmental alternations. The latest research on early-onset gastric cancer are trying to explain molecular and genetic basis, because young patients are less exposed to environmental factors predisposing to cancer. In the general population, Helicobacter pylori, has been particularly associated with intestinal subtype of gastric cancers. The significant association of Helicobacter pylori infection in young patients with gastric cancers suggests that the bacterium has an etiologic role in both diffuse and intestinal subtypes of early-onset gastric cancers. In this paper we would like to ascertain the possible role of Helicobacter pylori infection in the development of gastric carcinoma in young patients. The review summarizes recent literature on early-onset gastric cancers with special reference to Helicobacter pylori infection.

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          Helicobacter pylori infection.

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            Unidentified curved bacilli on gastric epithelium in active chronic gastritis.

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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

                Journal
                Oncotarget
                Oncotarget
                Oncotarget
                ImpactJ
                Oncotarget
                Impact Journals LLC
                1949-2553
                24 July 2018
                24 July 2018
                : 9
                : 57
                : 31146-31162
                Affiliations
                1 Department of Human Anatomy, Medical University of Lublin, Poland
                2 Department of Surgery with Trauma, Orthopaedic and Urological Subunit, Independent Public Health Care Center of the Ministry of Interior and Administration in Lublin, Poland
                3 Department of Surgical Oncology, Medical University of Lublin, Poland
                4 Department of Surgery, St. John's Cancer Center, Lublin, Poland
                Author notes
                Correspondence to: Robert Sitarz, r.sitarz@ 123456umlub.pl
                [*]

                These authors have contributed equally to this work

                Article
                25757
                10.18632/oncotarget.25757
                6089554
                30123433
                768cba48-f0fd-476c-bf5e-c0006cb2612e
                Copyright: © 2018 Pucułek et al.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 23 May 2018
                : 22 June 2018
                Categories
                Review

                Oncology & Radiotherapy
                early-onset gastric cancer,gastric cancer,h. pylori,genotypes,virulence factors

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