Negoi I. From infection to invasion: The role of deleted in malignant brain tumors 1 in Helicobacter pylori-driven gastric cancer. World J Clin Oncol 2025; 16(10): 108377 [PMID: 41178926 DOI: 10.5306/wjco.v16.i10.108377]
Corresponding Author of This Article
Ionut Negoi, MD, PhD, Associate Professor, Department of General Surgery, Carol Davila University of Medicine and Pharmacy Bucharest, Clinical Emergency Hospital of Bucharest, No. 8 Floreasca Street, Sector 1, Bucharest 014461, Romania. negoiionut@gmail.com
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Surgery
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Editorial
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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/
Oct 24, 2025 (publication date) through Nov 27, 2025
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World Journal of Clinical Oncology
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2218-4333
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Negoi I. From infection to invasion: The role of deleted in malignant brain tumors 1 in Helicobacter pylori-driven gastric cancer. World J Clin Oncol 2025; 16(10): 108377 [PMID: 41178926 DOI: 10.5306/wjco.v16.i10.108377]
World J Clin Oncol. Oct 24, 2025; 16(10): 108377 Published online Oct 24, 2025. doi: 10.5306/wjco.v16.i10.108377
From infection to invasion: The role of deleted in malignant brain tumors 1 in Helicobacter pylori-driven gastric cancer
Ionut Negoi
Ionut Negoi, Department of General Surgery, Carol Davila University of Medicine and Pharmacy Bucharest, Clinical Emergency Hospital of Bucharest, Bucharest 014461, Romania
Author contributions: Negoi I contributed to this study, designed the overall concept and outline of the manuscript, contributed to the discussion and design of the manuscript, contributed to the writing, and edited the manuscript, and review of the literature.
Conflict-of-interest statement: The author reports 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: Ionut Negoi, MD, PhD, Associate Professor, Department of General Surgery, Carol Davila University of Medicine and Pharmacy Bucharest, Clinical Emergency Hospital of Bucharest, No. 8 Floreasca Street, Sector 1, Bucharest 014461, Romania. negoiionut@gmail.com
Received: April 14, 2025 Revised: May 24, 2025 Accepted: September 2, 2025 Published online: October 24, 2025 Processing time: 195 Days and 6.9 Hours
Abstract
Gastric cancer (GC) remains a major health challenge worldwide, with Helicobacter pylori (H. pylori) infection playing a key role in its development. H. pylori creates a mutagenic environment in the stomach by causing chronic inflammation, oxidative DNA damage, inducing DNA double-strand breaks, and disrupting DNA repair mechanisms and cell cycle checkpoints. Cytotoxin-associated gene A is the main carcinogenic component of H. pylori and interacts with signaling pathways to promote carcinogenesis. Deleted in malignant brain tumors 1 (DMBT1), a potential tumor suppressor gene, shows variable expression patterns in GC. DMBT1 is frequently downregulated in well-differentiated gastric adenocarcinomas but upregulated in other GC types. The correlation between DMBT1 expression and H. pylori infection is important, as maintained DMBT1 expression in precancerous states may protect against gastric carcinogenesis, while its downregulation may facilitate tumor progression. DMBT1 functions as a pattern recognition receptor that binds to H. pylori and other pathogens and modulates inflammatory and immune responses. H. pylori colonization of gastric mucosa can induce an inflammatory microenvironment, which influences tumor suppressor gene expression, including DMBT1. Understanding the interactions between DMBT1 and H. pylori may reveal new therapeutic targets and preventive strategies for H. pylori-associated gastric disease.
Core Tip: Gastric cancer (GC) remains a major global health issue closely linked to Helicobacter pylori (H. pylori) infection, which induces chronic inflammation, oxidative DNA damage, and disrupts cell cycle regulation. Cytotoxin-associated gene A plays a significant role in carcinogenesis. Deleted in malignant brain tumors 1 (DMBT1), a potential tumor suppressor, shows variable expression in GC, often being downregulated in well-differentiated adenocarcinomas and upregulated in other subtypes. DMBT1 interacts directly with H. pylori to modulate the immune response. Preserved DMBT1 expression may protect against gastric carcinogenesis, whereas its downregulation may facilitate tumor progression. Understanding the DMBT1-H. pylori interaction could help identify new therapeutic strategies for the prevention and treatment of GC.
