Maity R, Dhali A, Biswas J. Is Helicobacter pylori infection protective against esophageal cancer? World J Gastroenterol 2024; 30(38): 4168-4174 [PMID: 39493327 DOI: 10.3748/wjg.v30.i38.4168]
Corresponding Author of This Article
Arkadeep Dhali, MBBS, MPH, PGCert Clin Ed, FRSPH, NIHR Academic Clinical Fellow, Department of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, United Kingdom. arkadipdhali@gmail.com
Research Domain of This Article
Medicine, General & Internal
Article-Type of This Article
Editorial
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. Oct 14, 2024; 30(38): 4168-4174 Published online Oct 14, 2024. doi: 10.3748/wjg.v30.i38.4168
Is Helicobacter pylori infection protective against esophageal cancer?
Rick Maity, Arkadeep Dhali, Jyotirmoy Biswas
Rick Maity, General Medicine, Institute of Post Graduate Medical Education and Research, Kolkata 700020, India
Arkadeep Dhali, Department of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Royal Hallamshire Hospital, Sheffield S10 2JF, United Kingdom
Arkadeep Dhali, School of Medicine and Population Health, University of Sheffield, Sheffield S10 2HQ, United Kingdom
Arkadeep Dhali, Deanery of Clinical Sciences, University of Edinburgh, Edinburgh EH16 4SB, United Kingdom
Jyotirmoy Biswas, Department of General Medicine, College of Medicine and Sagore Dutta Hospital, Kolkata 700058, India
Co-first authors: Rick Maity and Arkadeep Dhali.
Author contributions: Maity R conducted literature review and wrote the primary manuscript; Dhali A conceptualized the article; Biswas J conducted literature review and wrote the primary manuscript; All authors agreed with the final version of the manuscript.
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: Arkadeep Dhali, MBBS, MPH, PGCert Clin Ed, FRSPH, NIHR Academic Clinical Fellow, Department of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, United Kingdom. arkadipdhali@gmail.com
Received: August 1, 2024 Revised: September 10, 2024 Accepted: September 14, 2024 Published online: October 14, 2024 Processing time: 58 Days and 16.2 Hours
Abstract
Helicobacter pylori (H. pylori) infection affects a substantial proportion of the global population and causes various gastric disorders, including gastric cancer. Recent studies have found an inverse relationship between H. pylori infection and esophageal cancer (EC), suggesting a protective role against EC. This editorial focuses on the possible mechanisms underlying the role of H. pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the practicality of H. pylori eradication. EC has two major subtypes: Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), which have different etiologies and risk factors. Gut microbiota can contribute to EC via inflammation-induced carcinogenesis, immunomodulation, lactagenesis, and genotoxin production. H. pylori infection is said to be inversely related to EAC, protecting against EAC by inducing atrophic gastritis, altering serum ghrelin levels, and triggering cancer cell apoptosis. Though H. pylori infection has no significant association with ESCC, COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H. pylori-infected individuals. There are concerns regarding a plausible increase in EC after H. pylori eradication treatments. However, H. pylori eradication is not associated with an increased risk of EC, making it safe from an EC perspective.
Core Tip: Helicobacter pylori (H. pylori) infection, while being a risk factor for gastric cancer, may afford protection against esophageal cancer (EC). The two major subtypes of EC, i.e., esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC), have different etiologies and risk factors. Recent studies have unequivocally established the inverse association between H. pylori infection and EAC, however there was no significant association with ESCC. H. pylori infection may protect against EAC by inducing atrophic gastritis, altering serum ghrelin levels, and triggering cancer cell apoptosis. Contrary to prevailing concerns, H. pylori eradication does not increase the risk of EC.
