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      Alteration in Serum Levels of Tumor Necrosis Factor Alpha is associated with Histopathologic Progression of Gastric Cancer

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          Abstract

          Background:

          The role of inflammatory cytokines, such as TNF-α and IL-8, in gastric carcinogenesis has been investigated, but their impact remains to be further elucidated.

          Methods:

          In this study, we measured the serum concentrations of these cytokines and H. pylori serostatus in dyspeptic patients, presenting with normal mucosa (NM = 53), chronic gastritis (CG = 94), and gastric cancer (GC = 82), by ELISA.

          Results:

          Moderate levels of TNF-α were detected in the NM group (19.9 ± 19.5 pg/ml), which were nearly doubled in patients with CG (35.7 ± 28.0 pg/ml) and drastically declined in GC patients (1.8 ± 5.9 pg/ml). The serum levels of IL-8, however, were not statistically different amongst these three groups.

          Conclusion:

          TNF-α serum concentration seemed to undergo up- and downregulation, when moving from NM to CG and from CG to GC, respectively. If confirmed in a prospective study, this cytokine can behave as a serum indicator of gastric inflammation and malignant transformation.

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          Most cited references25

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          Molecular and cellular insights into T cell exhaustion.

          In chronic infections and cancer, T cells are exposed to persistent antigen and/or inflammatory signals. This scenario is often associated with the deterioration of T cell function: a state called 'exhaustion'. Exhausted T cells lose robust effector functions, express multiple inhibitory receptors and are defined by an altered transcriptional programme. T cell exhaustion is often associated with inefficient control of persisting infections and tumours, but revitalization of exhausted T cells can reinvigorate immunity. Here, we review recent advances that provide a clearer molecular understanding of T cell exhaustion and reveal new therapeutic targets for persisting infections and cancer.
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            Epidemiology of gastric cancer: global trends, risk factors and prevention

            Gastric cancer remains one of the most common and deadly cancers worldwide, especially among older males. Based on GLOBOCAN 2018 data, stomach cancer is the 5th most common neoplasm and the 3rd most deadly cancer, with an estimated 783,000 deaths in 2018. Gastric cancer incidence and mortality are highly variable by region and highly dependent on diet and Helicobacter pylori infection. While strides in preventing and treating H. pylori infection have decreased the overall incidence of gastric cancer, they have also contributed to an increase in the incidence of cardia gastric cancer, a rare subtype of the neoplasm that has grown 7-fold in the past decades. A better understanding of the etiology and risk factors of the disease can help reach a consensus in approaching H. pylori infection. Dietary modification, smoking cessation, and exercise hold promise in preventing gastric cancer, while genetic testing is enabling earlier diagnosis and thus greater survival.
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              The gastric precancerous cascade.

              Invasive gastric carcinoma is preceded by a cascade of precancerous lesions. The first recognized histologic change is active chronic inflammation, which may persist as such: non-atrophic chronic gastritis (no gland loss), or advance to multifocal atrophic gastritis (MAG), the first real step in the precancerous cascade. The following steps are: intestinal metaplasia (first "complete" and then "incomplete"); dysplasia, first low grade and then high grade (equivalent to "carcinoma in situ"). The following step is invasive carcinoma, which is thought to be associated with degradation of the intercellular matrix. © 2011 The Authors. Journal of Digestive Diseases © 2011 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and Blackwell Publishing Asia Pty Ltd.
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                Author and article information

                Journal
                Iran Biomed J
                Iran Biomed J
                IBJ
                Iranian Biomedical Journal
                Pasteur Institute of Iran (Tehran, Iran )
                1028-852X
                2008-823X
                January 2023
                21 December 2022
                : 27
                : 1
                : 72-78
                Affiliations
                [1 ]HPGC Research Group, Medical Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran;
                [2 ]Gastroenterology Department, Amiralam Hospital, Tehran University of Medical Sciences, Tehran, Iran;
                [3 ]Cancer Institute, Tehran University of Medical Sciences, Tehran, Iran;
                [4 ]Institut Pasteur, Unit of Helicobacter Pathogenesis, CNRS UMR2001, 25-28 Rue du Dr Roux, 75724 Paris Cedex 15, France;
                [5 ]Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
                Author notes
                [* ]Corresponding Author: Marjan Mohammadi HPGC Research Group, Department of Medical Biotechnology, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran; E-mail: marjan.mohammadi@pasteur.ac.ir; marjan.mohammadi2010@gmail.com
                Article
                10.52547/ibj.3847
                9971713
                36624700
                585d157c-2154-4223-8236-44551a5bd794

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 October 2022
                : 19 December 2022
                Categories
                Short Communication

                inflammation,interleukin-8,cytokines,tumor necrosis factor-alpha

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