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      Helicobacter pylori Virulence Factor Cytotoxin-Associated Gene A (CagA)-Mediated Gastric Pathogenicity

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          Abstract

          Helicobacter pylori causes persistent infection in the gastric epithelium of more than half of the world’s population, leading to the development of severe complications such as peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Several virulence factors, including cytotoxin-associated gene A (CagA), which is translocated into the gastric epithelium via the type 4 secretory system (T4SS), have been indicated to play a vital role in disease development. Although infection with strains harboring the East Asian type of CagA possessing the EPIYA-A, -B, and -D sequences has been found to potentiate cell proliferation and disease pathogenicity, the exact mechanism of CagA involvement in disease severity still remains to be elucidated. Therefore, we discuss the possible role of CagA in gastric pathogenicity.

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          Most cited references128

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          New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer

          Epithelial-mesenchymal transition (EMT) is a cellular programme that is known to be crucial for embryogenesis, wound healing and malignant progression. During EMT, cell-cell and cell-extracellular matrix interactions are remodelled, which leads to the detachment of epithelial cells from each other and the underlying basement membrane, and a new transcriptional programme is activated to promote the mesenchymal fate. In the context of neoplasias, EMT confers on cancer cells increased tumour-initiating and metastatic potential and a greater resistance to elimination by several therapeutic regimens. In this Review, we discuss recent findings on the mechanisms and roles of EMT in normal and neoplastic tissues, and the cell-intrinsic signals that sustain expression of this programme. We also highlight how EMT gives rise to a variety of intermediate cell states between the epithelial and the mesenchymal state, which could function as cancer stem cells. In addition, we describe the contributions of the tumour microenvironment in inducing EMT and the effects of EMT on the immunobiology of carcinomas.
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            Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis.

            The epidemiology of Helicobacter pylori infection has changed with improvements in sanitation and methods of eradication. We performed a systematic review and meta-analysis to evaluate changes in the global prevalence of H pylori infection.
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              Stem cells, cancer, and cancer stem cells.

              Stem cell biology has come of age. Unequivocal proof that stem cells exist in the haematopoietic system has given way to the prospective isolation of several tissue-specific stem and progenitor cells, the initial delineation of their properties and expressed genetic programmes, and the beginnings of their utility in regenerative medicine. Perhaps the most important and useful property of stem cells is that of self-renewal. Through this property, striking parallels can be found between stem cells and cancer cells: tumours may often originate from the transformation of normal stem cells, similar signalling pathways may regulate self-renewal in stem cells and cancer cells, and cancer cells may include 'cancer stem cells' - rare cells with indefinite potential for self-renewal that drive tumorigenesis.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                08 October 2020
                October 2020
                : 21
                : 19
                : 7430
                Affiliations
                [1 ]Department of Microbiology, Chitwan Medical College, Bharatpur 44200, Nepal; ansari.shamshul@ 123456cmc.edu.np
                [2 ]Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Oita 879-5593, Japan
                [3 ]Global Oita Medical Advanced Research Center for Health (GO-MARCH), Yufu, Oita 879-5593, Japan
                [4 ]Department of Medicine, Gastroenterology and Hepatology Section, Baylor College of Medicine, Houston, TX 77030, USA
                [5 ]Borneo Medical and Health Research Centre, Universiti Malaysia Sabah, Kota Kinabalu, Sabah 88400, Malaysia
                Author notes
                [* ]Correspondence: yyamaoka@ 123456oita-u.ac.jp ; Tel.: +81-97-586-5740; Fax: +81-97-586-5749
                Author information
                https://orcid.org/0000-0003-1846-1377
                https://orcid.org/0000-0002-1222-5819
                Article
                ijms-21-07430
                10.3390/ijms21197430
                7582651
                33050101
                9b96c364-c09b-440d-bbff-8cfb76c681ce
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 21 September 2020
                : 06 October 2020
                Categories
                Review

                Molecular biology
                h. pylori,virulence factor,cag pathogenicity island,caga,gastric cancer
                Molecular biology
                h. pylori, virulence factor, cag pathogenicity island, caga, gastric cancer

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