Liu C, Wu CH, Jia YB, Qiu JX, Li XY, Ling JH. Gastric organoids: A promising model for studying “inflammation-cancer” transition in atrophic gastritis. World J Clin Oncol 2025; 16(11): 110453 [DOI: 10.5306/wjco.v16.i11.110453]
Corresponding Author of This Article
Jiang-Hong Ling, Department of Gastroenterology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, No. 185 Pu’an Road, Huangpu District, Shanghai 201203, China. ljh18817424778@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
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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/
Nov 24, 2025 (publication date) through Nov 21, 2025
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Journal Information of This Article
Publication Name
World Journal of Clinical Oncology
ISSN
2218-4333
Publisher of This Article
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Liu C, Wu CH, Jia YB, Qiu JX, Li XY, Ling JH. Gastric organoids: A promising model for studying “inflammation-cancer” transition in atrophic gastritis. World J Clin Oncol 2025; 16(11): 110453 [DOI: 10.5306/wjco.v16.i11.110453]
Chang Liu, Chen-Heng Wu, Yue-Bo Jia, Xin-Yuan Li, Jiang-Hong Ling, Department of Gastroenterology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Jun-Xin Qiu, Department of Traditional Chinese Medicine, Jinshan Hospital of Fudan University, Shanghai 201508, China
Co-first authors: Chang Liu and Chen-Heng Wu.
Co-corresponding authors: Xin-Yuan Li and Jiang-Hong Ling.
Author contributions: Liu C and Wu CH conceived the review topic, designed the structure, and drafted the manuscript; Jia YB and Qu JX created the figures and tables; Li XY and Ling JH provided senior oversight, edited the full text, and approved the final version; Liu C and Wu CH contributed equally to this manuscript and should be regarded as the co-first authors; Li XY and Ling JH contributed equally to this manuscript and should be regarded as the co-corresponding authors. All authors read and approved the final manuscript.
Supported by National Traditional Chinese Medicine Advantageous Specialty Project of National Administration of Traditional Chinese Medicine; and Shuguang Hospital Siming Foundation Research Special Project, No. SGKJ-202304.
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: Jiang-Hong Ling, Department of Gastroenterology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, No. 185 Pu’an Road, Huangpu District, Shanghai 201203, China. ljh18817424778@163.com
Received: June 9, 2025 Revised: July 21, 2025 Accepted: October 27, 2025 Published online: November 24, 2025 Processing time: 167 Days and 18.5 Hours
Abstract
Current experimental models struggle to simulate the complex process of the transformation from atrophic gastritis to gastric cancer, while gastric organoid technology, especially region-specific modeling, provides a more precise in vitro platform for studying this carcinogenic mechanism. Helicobacter pylori activates carcinogenic signaling pathways through virulence factors, inducing DNA damage, epigenetic dysregulation, and immune microenvironment imbalance, driving inflammation-cancer conversion. Intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia serve as critical precursor lesions, gradually developing into dysplasia and adenocarcinoma under the influence of chronic inflammation and genetic instability through intestinal cell transformation and high trefoil factor 2-expressing cell expansion. The immune suppression, metabolic reprogramming, and matrix remodeling within the tumor microenvironment collaboratively create a pro-cancer ecosystem that accelerates inflammation-carcinogenesis transformation. The gastric organoid model successfully simulates the spatiotemporal dynamics of the carcinogenesis process in atrophic gastritis, and its future integration with single-cell omics, real-time imaging technologies, and artificial intelligence technologies could provide a more precise platform for elucidating molecular mechanisms and screening intervention strategies. These advances position gastric organoids as pivotal tools for clinical translation, enabling personalized risk stratification, early intervention targeting precancerous transitions, and ex vivo prediction of patient-specific therapeutic responses to guide precision management of gastric cancer.
Core Tip: Existing models are difficult to simulate the complex process of atrophic gastritis to gastric cancer, and gastric organoid technology provides a more accurate platform for studying this mechanism. Helicobacter pylori infection triggers activation of key oncogenic signaling pathways, DNA damage, and epigenetic alterations through its virulence factors and induced persistent inflammation. The gradual development of intestinal metaplasia and spasmodic polypeptide-expressing metaplasia accelerates the completion of inflammation-cancer transition under the combined action of tumor microenvironment of immunosuppression, metabolic abnormalities, and matrix remodeling. The gastric organoid model successfully simulates the spatiotemporal dynamics of inflammation-cancer transition, and provides a powerful in vitro research platform.
