Iizasa H, Kartika AV, Fekadu S, Okada S, Onomura D, Wadi AFAA, Khatun MM, Moe TM, Nishikawa J, Yoshiyama H. Development of Epstein-Barr virus-associated gastric cancer: Infection, inflammation, and oncogenesis. World J Gastroenterol 2022; 28(44): 6249-6257 [PMID: 36504553 DOI: 10.3748/wjg.v28.i44.6249]
Corresponding Author of This Article
Hironori Yoshiyama, MD, PhD, Professor, Department of Microbiology, Shimane University Faculty of Medicine, 89-1 Enyacho, Izumo 693-8501, Shimane, Japan. yosiyama@med.shimane-u.ac.jp
Research Domain of This Article
Microbiology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Nov 28, 2022; 28(44): 6249-6257 Published online Nov 28, 2022. doi: 10.3748/wjg.v28.i44.6249
Development of Epstein-Barr virus-associated gastric cancer: Infection, inflammation, and oncogenesis
Hisashi Iizasa, Andy Visi Kartika, Sintayehu Fekadu, Shunpei Okada, Daichi Onomura, Afifah Fatimah Azzahra Ahmad Wadi, Mosammat Mahmuda Khatun, Thin Myat Moe, Jun Nishikawa, Hironori Yoshiyama
Hisashi Iizasa, Andy Visi Kartika, Sintayehu Fekadu, Shunpei Okada, Daichi Onomura, Afifah Fatimah Azzahra Ahmad Wadi, Mosammat Mahmuda Khatun, Thin Myat Moe, Hironori Yoshiyama, Department of Microbiology, Shimane University Faculty of Medicine, Izumo 693-8501, Shimane, Japan
Andy Visi Kartika, Faculty of Medicine, Muslim University of Indonesia, Makassar 90231, Indonesia
Sintayehu Fekadu, Department of Medical Microbiology and Parasitology, Hawassa University, College of Medicine and Health Science, Hawassa 1560, Ethiopia
Jun Nishikawa, Faculty of Laboratory Science, Yamaguchi University Graduate School of Medicine, Ube 755-8505, Japan
Author contributions: Iizasa H and Okada S contributed to the manuscript writing; Kartika AV, Fekadu S, and Wadi AFAA contributed to the graphic writing; Onomura D, Khatun MM and Moe TM contributed to literature search; Nishikawa J contributed to the study idea and study design; Yoshiyama H contributed to the study idea, study design, manuscript writing, and the final revision of the manuscript.
Supported byGrant-in-Aid for Scientific Research From the Ministry of Education, Culture, Science and Technology of Japan, No. 21K07054 (Hironori Yoshiyama) and No. 22K07101 (Hisashi Iizasa).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hironori Yoshiyama, MD, PhD, Professor, Department of Microbiology, Shimane University Faculty of Medicine, 89-1 Enyacho, Izumo 693-8501, Shimane, Japan. yosiyama@med.shimane-u.ac.jp
Received: September 9, 2022 Peer-review started: September 9, 2022 First decision: September 29, 2022 Revised: October 24, 2022 Accepted: November 9, 2022 Article in press: November 9, 2022 Published online: November 28, 2022 Processing time: 76 Days and 10.8 Hours
Abstract
Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) cells originate from a single-cell clone infected with EBV. However, more than 95% of patients with gastric cancer have a history of Helicobacter pylori (H. pylori) infection, and H. pylori is a major causative agent of gastric cancer. Therefore, it has long been argued that H. pylori infection may affect the development of EBVaGC, a subtype of gastric cancer. Atrophic gastrointestinal inflammation, a symptom of H. pylori infection, is observed in the gastric mucosa of EBVaGC. Therefore, it remains unclear whether H. pylori infection is a cofactor for gastric carcinogenesis caused by EBV infection or whether H. pylori and EBV infections act independently on gastric cancer formation. It has been reported that EBV infection assists in the onco-genesis of gastric cancer caused by H. pylori infection. In contrast, several studies have reported that H. pylori infection accelerates tumorigenesis initiated by EBV infection. By reviewing both clinical epidemiological and experimental data, we reorganized the role of H. pylori and EBV infections in gastric cancer formation.
Core Tip: Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) tumor cells originate from a single cell clone infected with EBV. In contrast, it is reported that more than 95% of patients with gastric cancer have a history of Helicobacter pylori (H. pylori) infection. Accordingly, it has long been argued that H. pylori infection may have some effect on the development of EBVaGC, a subtype of gastric cancer. It is also a mystery that the number of gastric cancer patients is higher in Asia, South America, and the Middle East. We will reorganize the role of H. pylori and EBV infections in gastric cancer formation.
