[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-352289-105":59,"doc-detail-352289-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","molecular-insights-into-helicobacter-pylori-induced-gastritis-and-gastric-cancer-review","Molecular Insights into Helicobacter pylori-Induced Gastritis and Gastric Cancer - Review","","Helicobacter pylori (H. pylori) is a widespread and persistent bacterial infection that efficiently colonizes the human stomach. It drives gastric disease development, including gastric lymphoma and adenocarcinoma, through a pathogenic cascade marked by prolonged inflammation and oxidative stress. Persistent infection promotes immune dysregulation, epithelial injury, and tissue remodeling, followed by epigenetic changes such as DNA methylation, histone modifications, and altered non-coding RNA expression that increase susceptibility to dysplasia and cancer. This review summarizes recent molecular advances and highlights therapeutic implications.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/molecular-insights-into-helicobacter-pylori-induced-gastritis-and-gastric-cancer-review/352289/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/molecular-insights-into-helicobacter-pylori-induced-gastritis-and-gastric-cancer-review/352289.png","ImageObject",300,407,{"name":92,"@type":93},"Olivia Brown","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-09-27","2026-09-22",true,{"@type":102,"interactionType":103,"userInteractionCount":81},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"How does Helicobacter pylori contribute to gastric cancer development?","Question",{"text":112,"@type":113},"Helicobacter pylori infection causes prolonged inflammation and oxidative stress, leading to immune dysregulation, epithelial injury, and tissue remodeling. Repeated inflammatory and damage cycles then drive epigenetic alterations that increase susceptibility to dysplasia and cancer.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What molecular and epigenetic changes are highlighted in H. pylori-induced gastritis?",{"text":117,"@type":113},"The review emphasizes changes in DNA methylation, histone modifications, and non-coding RNA expression. These alterations make gastric epithelial cells more prone to further aberrations, including dysplasia and cancer.",{"name":119,"@type":110,"acceptedAnswer":120},"What is the role of immune cells in the disease-prone environment?",{"text":121,"@type":113},"H. pylori infection creates a milieu shaped by cooperation between immune cells and non-immune cells. Both innate and adaptive immune cells become inappropriately activated, contributing to epithelial injury and remodeling.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},352289,1790251338,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":81,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145},16904993612988,"https://ap-avatar.wpscdn.com/davatar_a8503ba1806abce46bf441b54a3ca4cd","Review  \nMolecular Insights into Helicobacter pylori-Induced Gastritis and Gastric Cancer  \nSilvia Salvatori 1,2, Irene Marafini 1,2, Pasquale De Vico 3, Antonio Fonsi 1 and Giovanni Monteleone 1,2, *  \nAcademic Editor: Hidekazu Suzuki  \nReceived: 14 December 2025  \nRevised: 14 January 2026  \nAccepted: 20 January 2026  \nPublished: 21 January 2026  \nCopyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 Department of Systems Medicine, University of Rome “Tor Vergata”, 00133 Rome, Italy;  \nsilvia.salvatori@ptvonline.it (S.S.); irene.marafini@ptvonline.it (I.M.); antonio.fonsi@ptvonline.it (A.F.)  \n2 Gastroenterology Unit, Fondazione Policlinico “Tor Vergata”, 00133 Rome, Italy  \n3 Department of Anaesthesia, University of Rome “Tor Vergata”, 00133 Rome, Italy; [pasquale.devico@ptvonline.it](pasquale.devico@ptvonline.it)  \n* Correspondence: [gi.monteleone@med.uniroma2.it](gi.monteleone@med.uniroma2.it); Tel.: +39-06-20903702; Fax: +39-06-72596391  \nSimple Summary  \nHelicobacter pylori (H. pylori) is a widespread bacterium that infects the human stomach, contributing to various diseases, including peptic ulcers and gastric cancer. The infection triggers a long-lasting inflammatory response, which can eventually damage the stomach’s epithelial cells and promote genetic changes, such as alterations in DNA methylation and histone modifications that make the cells more likely to become cancerous. This review examines the molecular mechanisms behind H. pylori-induced gastritis and its role in the development of gastric cancer, highlighting how various immune cells and non-immune cells work together to create a disease-prone environment.  \nAbstract  \nHelicobacter pylori (H. pylori) is recognized as one of the most widespread and persistent bacterial infections globally, with a remarkable ability to colonize the human stomach. This pathogen is a major contributor to the development of gastric diseases, including gastric lymphoma and adenocarcinoma. The H. pylori infection triggers a complex pathogenic cascade within the gastric environment, characterized by prolonged inflammation and heightened oxidative stress, which fosters a milieu of immune dysregulation, where both innate and adaptive immune cells become activated inappropriately, thereby leading to epithelial injury and subsequent remodeling of the gastric tissue. As the infection persists, repeated cycles of inflammation and epithelial damage contribute to the development of epigenetic alterations, including changes in DNA methylation, histone modifications, and non-coding RNA expression, all of which render the gastric epithelium more susceptible to further aberrations, including dysplasia and cancer. In this article, we review the latest advances in understanding the molecular mechanisms of H. pylori-induced gastritis and its role in the progression of gastric cancer, offering new perspectives on the complex biology of this infection and its potential therapeutic implications for preventing the development of gastric malignancies.  \nKeywords: H. pylori; gastric cancer; chronic gastritis  \n1. Introduction  \nHelicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative bacterium that has evolved to colonize the acidic environment of the human stomach. Since its initial identification in the early 1980s, H. pylori has been recognized as the leading cause of chronic gastritis  \nand remains the only bacterial species classified by the International Agency for Research on Cancer (IARC) as a Group I carcinogen [1]. Although many H. pylori-infected individuals never develop symptoms, a subset of them can experience serious complications, including peptic ulcers, gastric adenocarcinoma, and, less commonly, mucosa-associated lymphoid tissue (MALT) lymphoma [2–6] . Although pioneering epidemiological studies showed that H. pylori infect","cbCaiqWNHU81D2mJ","https://ap.wps.com/l/cbCaiqWNHU81D2mJ","pdf",972832,15,"English","# Simple Summary\n# Abstract\n# Keywords\n# 1. Introduction","[{\"question\":\"How does Helicobacter pylori contribute to gastric cancer development?\",\"answer\":\"Helicobacter pylori infection causes prolonged inflammation and oxidative stress, leading to immune dysregulation, epithelial injury, and tissue remodeling. Repeated inflammatory and damage cycles then drive epigenetic alterations that increase susceptibility to dysplasia and cancer.\"},{\"question\":\"What molecular and epigenetic changes are highlighted in H. pylori-induced gastritis?\",\"answer\":\"The review emphasizes changes in DNA methylation, histone modifications, and non-coding RNA expression. These alterations make gastric epithelial cells more prone to further aberrations, including dysplasia and cancer.\"},{\"question\":\"What is the role of immune cells in the disease-prone environment?\",\"answer\":\"H. pylori infection creates a milieu shaped by cooperation between immune cells and non-immune cells. Both innate and adaptive immune cells become inappropriately activated, contributing to epithelial injury and remodeling.\"}]","Molecular Insights into Helicobacter pylori-Induced Gastritis and Gastric Cancer - Review | PDF",1790098768,38]