[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-360767-105":59,"doc-detail-360767-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","gastric-intestinal-metaplasia-unraveling-the-multifactorial-pathogenesis-and-advancing-risk-stratification-for-gastric-cancer-prevention","Gastric intestinal metaplasia - unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention","","Gastric intestinal metaplasia (GIM) is a precancerous lesion in which normal gastric mucosa is replaced by intestinal-type epithelium, acting as a key intermediate step in the Correa cascade toward intestinal-type gastric cancer. This review consolidates histological classification and global epidemiology, then analyzes multifactorial risk factors and mechanisms, including Helicobacter pylori–host interactions, cellular reprogramming (notably pyloric metaplasia and SPEM), microbial dysbiosis, and immune microenvironment changes. It also summarizes validated and emerging biomarkers to improve prediction of malignant transformation and enable more precise prevention strategies.",{"@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":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/gastric-intestinal-metaplasia-unraveling-the-multifactorial-pathogenesis-and-advancing-risk-stratification-for-gastric-cancer-prevention/360767/",{"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/gastric-intestinal-metaplasia-unraveling-the-multifactorial-pathogenesis-and-advancing-risk-stratification-for-gastric-cancer-prevention/360767.png","ImageObject",300,407,{"name":92,"@type":93},"Bulrr","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-27","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":52},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What is gastric intestinal metaplasia (GIM) and why is it important for gastric cancer prevention?","Question",{"text":112,"@type":113},"GIM is a precancerous lesion where gastric mucosa is replaced by intestinal-type epithelium. It represents a critical window in the Correa cascade for early clinical intervention to prevent progression toward gastric cancer.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"Which factors and mechanisms contribute to GIM development and progression?",{"text":117,"@type":113},"GIM involves the interplay of Helicobacter pylori infection and host susceptibility, cellular reprogramming (including pyloric metaplasia and SPEM), microbial dysbiosis, and alterations in the immune microenvironment.",{"name":119,"@type":110,"acceptedAnswer":120},"How can biomarkers help with risk stratification in patients with GIM?",{"text":121,"@type":113},"The review summarizes validated and emerging biomarkers linked to GIM and their predictive value for malignant transformation, supporting more accurate identification of individuals at higher risk.","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},360767,1790197961,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":52,"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":36},5909892115043,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","Cellular and Molecular Life Sciences (2026) 83:267  \n[https://doi.org/10.1007/s00018-026-06249-3](https://doi.org/10.1007/s00018-026-06249-3)  \nCellular and Molecular Life Sciences  \nREVIEW  \nGastric intestinal metaplasia: unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention  \nYuxin He1,2,3 · Zilin Deng1,2,3 · Tongguo Shi1,4 · Weichang Chen2,3,5  \nReceived: 16 March 2026 / Revised: 22 April 2026 / Accepted: 30 April 2026 © The Author(s) 2026  \nAbstract  \nGastric intestinal metaplasia (GIM) is a precancerous lesion characterized by the replacement of normal gastric mucosa with intestinal-type epithelium. As a critical intermediate stage in the Correa cascade, which is the established model of stepwise progression toward intestinal-type gastric cancer (GC), GIM represents a key window for clinical intervention. A comprehensive understanding of the molecular and histopathological features underlying GIM pathogenesis is therefore essential for improving patient stratification and outcomes. This review synthesizes current evidence regarding the histological classification and global epidemiology of GIM, then dissect the multifactorial risk factors and underlying pathogenic mechanisms, including the intricate interplay of Helicobacter pylori infection, host susceptibility, cellular reprogramming (with an emphasis on pyloric metaplasia and SPEM), microbial dysbiosis, and immune microenvironment alterations. Furthermore, we summarize validated and emerging biomarkers associated with GIM and their predictive value for malignant transformation. By navigating these complexities, this review aims to provide a foundational framework for advancing precision medicine approaches to intercept the metaplasia-carcinoma sequence and ultimately reduce the global burden of gastric cancer.  \nKeywords Gastric intestinal metaplasia · Pyloric metaplasia · Biomarker · Gastric cancer  \n􀀍 Tongguo Shi [shitg@suda.edu.cn](shitg@suda.edu.cn)  \n􀀍 Weichang Chen [weichangchen@126.com](weichangchen@126.com)  \n1 Jiangsu Institute of Clinical Immunology, The First Affiliated Hospital of Soochow University, Suzhou, China  \n2 Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, China  \n3 Jiangsu Key Laboratory of Clinical Immunology, Soochow University, Suzhou, China  \n4 Jiangsu Institute of Clinical Immunology, The First Affiliated Hospital of Soochow University, 178 East Ganjiang Road, Suzhou 215000, China  \n5 Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou 215000, China  \nIntroduction  \nGastric cancer (GC) remains a leading cause of cancerrelated mortality worldwide, with intestinal-type adenocarcinoma representing the predominant histological form [1] . The pathogenesis of this malignancy is not an abrupt event but rather a protracted, multi-step process, classically delineated by the Correa cascade. This model describes the sequential progression from chronic gastritis to atrophic gastritis, intestinal metaplasia, dysplasia, and ultimately, invasive carcinoma [2, 3] . Within this continuum, gastric intestinal metaplasia (GIM) has emerged as a critical juncture, which is a histologically identifiable alteration where the native gastric epithelium is replaced by intestinal-like cells [4–6] .  \nThe clinical significance of GIM is twofold. On one hand, its presence unequivocally signals an increased risk for GC, with an estimated annual incidence of 0. 13% to 0.25%[7] . On the other hand, the Correa cascade is not a deterministic, one-way street. The process is dynamic,  \ncharacterized by periods of stability, potential regression, and, in some cases, rapid progression that may even bypass canonical stages [8–10] . This inherent plasticity positions GIM as a crucial window for early intervention. However, it also presents a profound clinical dilemma. Helicobacter pylori (H. pylori) eradication is most effective in preventing GC b","cbCaijDPmQUt7oQ5","https://ap.wps.com/l/cbCaijDPmQUt7oQ5","pdf",2299710,16,"English","# Introduction\n## GC risk in GIM\n# Gastric intestinal metaplasia: multifactorial pathogenesis\n## Biomarkers and risk stratification","[{\"question\":\"What is gastric intestinal metaplasia (GIM) and why is it important for gastric cancer prevention?\",\"answer\":\"GIM is a precancerous lesion where gastric mucosa is replaced by intestinal-type epithelium. It represents a critical window in the Correa cascade for early clinical intervention to prevent progression toward gastric cancer.\"},{\"question\":\"Which factors and mechanisms contribute to GIM development and progression?\",\"answer\":\"GIM involves the interplay of Helicobacter pylori infection and host susceptibility, cellular reprogramming (including pyloric metaplasia and SPEM), microbial dysbiosis, and alterations in the immune microenvironment.\"},{\"question\":\"How can biomarkers help with risk stratification in patients with GIM?\",\"answer\":\"The review summarizes validated and emerging biomarkers linked to GIM and their predictive value for malignant transformation, supporting more accurate identification of individuals at higher risk.\"}]","Gastric intestinal metaplasia - unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention | PDF",1790141484]