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doi: 10.18282/amor.v2.i3.144

EDITORIAL

Working towards a better understanding of Helicobacter pylorirelated gastric cancer’s biology Omar Abdel-Rahman Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Keywords: Helicobacter pylori; gastric cancer; carcinogenesis; genetic markers Citation: Abdel-Rahman, O. Working towards a better understanding of Helicobacter pylori-related gastric cancer’s biology. Adv Mod Oncol Res 2016; 2(3): 123; http://dx.doi.org/10.18282/amor.v2.i3.144. *Correspondence to: Omar Abdel-Rahman, Clinical Oncology Department, Faculty of Medicine, Ain Shams University, Lotfy Elsayed Street, Cairo, 113331, Egypt; [email protected]

Received: 09th June 2016; Published Online: 15th June 2016

G

astric cancer is a significant cause of cancer-related mortality and morbidity. In terms of disease etiology, it ranks as the fourth and fifth most common contributor of male and female cancer-related death, respectively[1]. A marked geographical variability has been observed for gastric cancer incidence, with the majority of cases reported in Eastern Europe, South America, and Asia[2]. This has been ascribed to environmental (e.g., H. pylori infection), dietary, as well as genetic factors[3]. H. pylori is considered as a definite carcinogen by the International Agency for Research on Cancer, and intestinal metaplasia has been suggested as the intermediate event in the development of H. pylori-related gastric cancer[4]. However, the molecular mechanism of this event needs to be further elucidated. In this issue of AMOR, a report from Ukraine’s Vinnitsa National Pigorov Memorial Medical University by Sergii Vernygorodskyi attempts to improve our current understanding of the molecular mechanism associated with H. pylori-related gastric carcinogenesis[5]. The investigator found that the activation of CDX2, along with the simultaneous inactivation and a decreased number of genes (e.g., SHH, SOX2, and RUNX3) responsible for gastric differentiation, is a probable cause that leads to the appearance of intestinal metaplasia. Therefore, this study serves as an important catalyst to promote further research on the molecular mechanism and programming of gastric cancer cells, in hopes of

gaining new knowledge in the prevention and treatment of gastric cancer.

Conflict of interest The author declares no potential conflict of interest with respect to the research, authorship, and/or publication of this article.

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Jemal A, Bray F, Center MM, Ferlay J, Ward E, et al. Global cancer statistics. CA Cancer J Clin 2011; 61(2): 69–90. doi: 10.3322/caac.20107. Parkin DM, Bray F, Ferlay J, Pisani, P. Global cancer statistics, 2002. CA Cancer J Clin 2005; 55(2): 74–108. doi: 10.3322/canjclin.55.2.74. Fitzgerald RC, Hardwick R, Huntsman D, Carneiro F, Guilford P, et al. Hereditary diffuse gastric cancer: Updated consensus guidelines for clinical management and directions for future research. J Med Genet 2010; 47(7): 436–444. doi: 10.1136/jmg.2009.074237. Abdel-Rahman O. Insulin-like growth factor pathway aberrations and gastric cancer; Evaluation of prognostic significance and assessment of therapeutic potentials. Med Oncol 2015; 32(1): 431. doi: 10.1007/s12032-0140431-8. Vernygorodskyi S. Helicobacter pylori as a crucial factor in intestinal metaplasia development of gastric mucosa. Adv Mod Oncol Res 2016; 2(3): 165–173. doi 10.18282/ amor.v2.i3.72.

Copyright © 2016 Abdel-Rahman O. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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