Pathology, research and practice最新文献

{"title":"Hypoxia-driven metabolic and molecular reprogramming: From tumor microenvironment to therapeutic interventions","authors":"Diksha Devi ,&nbsp;Kanchan Sharma ,&nbsp;Tabish Khan ,&nbsp;Hema Rani ,&nbsp;Rekha Rana ,&nbsp;Heena Sharma ,&nbsp;Parjinder Kaur ,&nbsp;Lokesh Prajapati ,&nbsp;Adil Rizwan ,&nbsp;Moses Allieu ,&nbsp;Sampita Pal ,&nbsp;Vishal Kumar ,&nbsp;Sunny Kumar","doi":"10.1016/j.prp.2025.156271","DOIUrl":"10.1016/j.prp.2025.156271","url":null,"abstract":"<div><div>Hypoxia, characterized by reduced oxygen availability, significantly contributes to cancer development by affecting tumor growth and spread. In fast-growing tumors, the scarcity of oxygen forces cancer cells to modify their molecular structure and metabolism to survive and multiply. These alterations are predominantly governed by hypoxia-inducible factors (HIFs), with HIF-1α and HIF-2α serving crucial roles in the activation of genes related to invasion, angiogenesis, metabolic reprogramming, and metastasis. Such changes promote tumor development in low-oxygen environments and enhance resistance to conventional therapies. Hypoxia influences various aspects of cancer progression, heightening the risk of malignancy and worsening prognosis. This study investigates the fundamental mechanisms by which hypoxia influences tumor biology, including the facilitation of the epithelial-to-mesenchymal transition (EMT), the enhancement of angiogenesis through vascular endothelial growth factor (VEGF), and the metabolic shift from oxidative phosphorylation to glycolysis. In this review, we aim to elucidate the complex interaction of metabolic and molecular mechanisms within the cancer microenvironment under hypoxic conditions, which not only fosters tumor growth but also contributes to therapeutic resistance, making hypoxia a critical factor in cancer treatment strategies.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156271"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next generation DNA sequencing data analysis and its application in clinical genomics","authors":"Abhijit Beura ,&nbsp;Gowrang Kasaba Manjunath ,&nbsp;Shweta Mahalingam ,&nbsp;Mangesh Sudhakar Rajguru ,&nbsp;Tikam Chand Dakal ,&nbsp;Abhishek Kumar","doi":"10.1016/j.prp.2025.156280","DOIUrl":"10.1016/j.prp.2025.156280","url":null,"abstract":"<div><div>Next-generation sequencing (NGS) has transformed genomics by enabling rapid, high-throughput analysis of DNA and RNA, driving significant progress across multiple fields, such as cancer research, rare disease diagnosis, and personalized medicine. This review discusses the wide-ranging applications of NGS, particularly in identifying genetic variants that guide the development of targeted therapies, improving patient outcomes. The NGS workflow involves crucial steps including data quality control, sequence alignment, and variant calling, supported by both open-source and commercial tools. Cloud-based platforms have further streamlined the storage, management, and processing of the vast datasets generated by NGS technologies. As NGS continues to evolve, ethical challenges, especially concerning genomic data privacy and informed consent, remain critical considerations. Looking ahead, the integration of multi-omics data and the advent of single-cell sequencing hold the potential to deepen our understanding of complex biological processes. Essential databases like dbSNP, COSMIC, and The Cancer Genome Atlas are key resources for interpreting NGS findings and their clinical significance. By effectively utilizing these tools and datasets, researchers can generate new genetic insights with far-reaching implications for advancing human health and understanding disease mechanisms.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156280"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chuanxing Qingfei Syrup ameliorates acute lung injury by suppressing BCL10 expression and blocking the IKK/IκBα/NF-κB pathway","authors":"Yuanyuan Song ,&nbsp;Heng Li ,&nbsp;Yanyun Zhao ,&nbsp;Chen Cheng ,&nbsp;Weiwei Zhang ,&nbsp;Yingying Sun ,&nbsp;Taiyu Jin","doi":"10.1016/j.prp.2025.156273","DOIUrl":"10.1016/j.prp.2025.156273","url":null,"abstract":"<div><h3>Background</h3><div>Acute lung injury (ALI) is a potentially lethal condition with a considerable mortality rate. This study aims to determine the protective effect of Chuanxing Qingfei Syrup (CQS) against ALI.</div></div><div><h3>Methods</h3><div>An ALI model was constructed by dropping lipopolysaccharide (LPS) into the trachea of mice, and mice were treated with low, medium, and high doses of CQS to evaluate the therapeutic effect of CQS. LPS-treated A549 cells were used to construct an <em>in vitro</em> ALI model, and low, medium, and high doses of CQS were used to treat A549 cells. The cytotoxicity and therapeutic efficacy of CQS were verified. Bioinformatic analysis was employed to predict the downstream targets of CQS. BCL10 expression in mouse lung tissues and A549 cells was detected. The phosphorylation level of IKKβ, IκBα, and NF-κB p65, and the nuclear translocation of NF-κB p65 were measured. BCL10 overexpression and treatment with the NF-κB pathway inhibitor PDTC were performed to explore their effects on A549 cell injury. Intranasal instillation of overexpressed BCL10 adeno-associated virus was performed to observe its effect on ALI mice.</div></div><div><h3>Results</h3><div>CQS effectively alleviated the infiltration of inflammatory cells, reduced levels of inflammatory factors, inhibited apoptosis, and alleviated lung edema in mice. CQS inhibited apoptosis in A549 cells. CQS inhibited BCL10, and BCL10 activated the IKK/IκBα/NF-κB pathway. Overexpression of BCL10 aggravated A549 cell injury and pathological changes in ALI mice. PDTC treatment mitigated LPS-induced injury in A549 cells overexpressing BCL10.</div></div><div><h3>Conclusion</h3><div>CQS inhibits ALI progression by targeting BCL10 and suppressing the IKK/IκBα/NF-κB pathway.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156273"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145364456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating transcriptomics and machine learning to predict ferroptosis-related genes and analyzing the role of GOT1 in gastric cancer progression","authors":"Xiao-Ling Wu ,&nbsp;Li-Ping Lei ,&nbsp;Shu-Rui Wu,&nbsp;Mei-Yan Chen,&nbsp;Yu-Qin Zhang,&nbsp;Yu-Ka Fu,&nbsp;Qiong-Dan Kang,&nbsp;Shan-Ti Lin,&nbsp;Pei Li,&nbsp;Zhang-Xing Chen","doi":"10.1016/j.prp.2025.156252","DOIUrl":"10.1016/j.prp.2025.156252","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Gastric cancer (GC) is one of the leading causes of cancer-related mortality worldwide. Despite advances in treatment, the prognosis for advanced GC remains poor, highlighting the need for new therapeutic targets. Ferroptosis, a form of programmed cell death characterized by iron-dependent lipid peroxidation, has emerged as a potential pathway for cancer therapy. This study aims to identify ferroptosis-related genes in GC using transcriptomics and machine learning, and to validate the role of one key gene, Glutamic-Oxaloacetic Transaminase 1 (GOT1), in GC progression.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;The Sangerbox platform was employed to analyze differentially expressed genes between GC tissues and adjacent non-cancerous tissues in the GSE184336 dataset. Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify co-expressed gene modules from the GSE184336 dataset and their associations with phenotypes. Support Vector Machine (SVM) and Random Forest (RF) regression algorithms were applied to screen for core target genes. Quantitative Real-Time PCR (qRT-PCR) was used to analyze mRNA expression, while western blotting and immunohistochemistry (IHC) assays were used to determine protein expression. Cell proliferation was assessed using a 5-Ethynyl-2’-deoxyuridine assay, and cell migration was analyzed using a Transwell assay. Flow cytometry was used to quantify cell death. Fluorometric and colorimetric assays were performed to analyze Reactive Oxygen Species (ROS) and Fe&lt;sup&gt;2 +&lt;/sup&gt; levels, respectively. A xenograft mouse model was used to evaluate the impact of GOT1 overexpression on tumor formation &lt;em&gt;in vivo&lt;/em&gt;. Haematoxylin and eosin (HE) staining was used to analyze the pathological conditions of tumors.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;The analysis of the GSE184336 dataset identified 2297 dysregulated genes in GC tissues compared to adjacent non-cancerous tissues. WGCNA revealed strong correlations between gene significance and module membership in the “green,” “ivory,” and “lightsteelblue1” modules, encompassing 350 genes. Subsequent analysis identified 14 intersection genes among the 2297 dysregulated genes in GC tissues, the 350 genes from WGCNA, and the 1467 genes related to ferroptosis. Machine learning algorithms and protein-protein interaction analysis identified IDH2, BGN, IGFBP7, and GOT1 as key genes. GOT1 expression was downregulated in GC tissues with the lowest error value. Overexpression of GOT1 inhibited GC cell proliferation, migration, and induced ferroptosis, whereas these effects were reversed by treatment with Fer-1. Further, GOT1 overexpression suppressed the malignant phenotype of GC cells in vivo.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;This study identified several ferroptosis-related genes in GC, with GOT1 being a critical regulator. Overexpression of GOT1 significantly inhibited GC cell proliferation and migration, and induced ferroptosis. These findings sugges","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156252"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"U2AF2 drives malignant progression and chemo-resistance in hepatocellular carcinoma through cooperating with SRSF1 to modulate CCND1 splice-variant expression","authors":"Peng Luo ,&nbsp;Shijie Dai ,&nbsp;Xingyuan Xu ,&nbsp;Gaoyu Liu,&nbsp;Fulong Wang,&nbsp;Jialun Li,&nbsp;Qin Xiong,&nbsp;Yang Wang,&nbsp;Chunmeng Shi","doi":"10.1016/j.prp.2025.156272","DOIUrl":"10.1016/j.prp.2025.156272","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is a common malignancy with high risk of recurrence and metastasis. Growing evidences reveal that aberrant mRNA splicing represents a crucial molecular characteristic of cancer, which produces numerous and complex transcript variants to drive cancer development and progression. Here, we identified the splicing factor U2AF2 as a promising oncogenic biomarker in HCC, and subsequently explored its biological role and mechanism. Through bioinformatics analysis and clinical verification, U2AF2 was found to be significantly elevated in HCC, showing a strong correlation with the pathological grade and patient outcomes. Subsequent investigations demonstrated that U2AF2 promoted HCC growth and metastasis both in vitro and in vivo. Mechanically, U2AF2 exerted its oncogenic functions by cooperating with SRSF1 to bind to the pre-mRNA of CCND1(Cyclin D1) and facilitate the generation of CCND1b isoform. Moreover, U2AF2 could potentially be utilized for the prediction of chemo-responsiveness. Its depletion sensitized HCC cells to Doxorubicin, a first-line chemotherapy agent for advanced HCC patients. Altogether, this study deepens our understanding of U2AF2 in mRNA splicing and provides a potential therapeutic target for HCC.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156272"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145364457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic insights into plant-derived natural compounds for the treatment of skin cancer: Targeting molecular signaling for therapeutic intervention","authors":"Ashutosh Pathak ,&nbsp;G. Surendra ,&nbsp;Sathvik Belagodu Sridhar ,&nbsp;Patibandla Jahnavi ,&nbsp;Jeetendra Kumar Gupta ,&nbsp;P. Balaji ,&nbsp;N. Juniorsundresh ,&nbsp;Konatham Teja Kumar Reddy ,&nbsp;Abdul Ajeed Mohathasim Billah ,&nbsp;Karthickeyan Krishnan","doi":"10.1016/j.prp.2025.156277","DOIUrl":"10.1016/j.prp.2025.156277","url":null,"abstract":"<div><div>Skin cancer, a prevalent global cancer, is primarily caused by chronic environmental exposures and cellular signaling pathway deregulation. Traditional therapies like radiation, chemotherapy, and surgery face toxicity, resistance, and recurrence issues. Natural compounds, with their diverse biological activity and minimal side effects, are increasingly recognized as potential therapeutic agents. This review explores the potential of natural compounds in treating skin cancer by modifying key molecular signaling pathways, including MAPK/ERK, PI3K/Akt, NF-κB, STAT3, and Wnt/β-catenin. Curcumin, resveratrol, quercetin, epigallocatechin gallate, and genistein are natural substances known to have potent anticancer effects by inhibiting cell proliferation, promoting apoptosis, and preventing metastasis. These substances regulate inflammation, prevent angiogenesis, enhance drug effectiveness, combat multidrug resistance, and have low toxicity to healthy skin cells, indicating potential therapeutic use. Additionally, their compatibility with current chemotherapeutic drugs underscores their significant role in combating drug resistance. The review underscores the importance of understanding the molecular mechanisms underlying phytochemicals' anticancer properties to facilitate their integration into modern treatment methods. Future initiatives should focus on clinical validation, increasing bioavailability, and targeting administration schemes to maximize the therapeutic potential of natural chemicals against skin cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156277"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145392056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Automated spatial analysis reveals proximity of human leukocyte antigen class I-positive tumor cells and CD8-positive cells of the tumor microenvironment in stage I seminoma","authors":"Takuto Ogasawara ,&nbsp;Terufumi Kubo ,&nbsp;Kenta Sasaki ,&nbsp;Naoki Shijubou ,&nbsp;Rena Morita ,&nbsp;Kenji Murata ,&nbsp;Kohei Hashimoto ,&nbsp;Tomohide Tsukahara ,&nbsp;Hiroko Asanuma ,&nbsp;Toshihiko Torigoe ,&nbsp;Reiko Watanabe ,&nbsp;Naoya Masumori ,&nbsp;Yoshihiko Hirohashi","doi":"10.1016/j.prp.2025.156270","DOIUrl":"10.1016/j.prp.2025.156270","url":null,"abstract":"<div><h3>Background</h3><div>The testis is an immune-privileged organ due to its lack of functional human leukocyte antigen (HLA) class I expression. However, the expression status of HLA class I in testicular seminoma, which is characterized histologically by lymphocytic infiltration, remains unclear.</div></div><div><h3>Materials and methods</h3><div>We performed immunohistochemistry to evaluate HLA class I expression and its spatial relationship with CD8-positive cells in 20 cases of stage I seminoma. Each specimen was scored manually and further analyzed using the HALO image analysis platform.</div></div><div><h3>Results</h3><div>Manual scoring and HALO analysis showed 80 % concordance. HLA class I expression was positive in 13 cases (65 %). Tumors were classified into three categories based on the expression levels. The number of infiltrating CD8-positive cells was significantly correlated with HLA class I expression. Spatial analysis revealed that tumors with higher HLA class I expression had shorter distances between HLA class I–positive tumor cells and CD8-positive cells.</div></div><div><h3>Conclusion</h3><div>Seminoma cells expressing HLA class I tended to be located in close proximity to CD8-positive T cells, suggesting a spatial relationship that might influence the tumor immune microenvironment.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156270"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTEN mutation status in uterine carcinosarcomas: A comprehensive overview and a new diagnostic approach","authors":"Maccio Livia ,&nbsp;Bragantini Emma ,&nbsp;Piermattei Alessia ,&nbsp;Santoro Angela ,&nbsp;Zannoni Gian Franco","doi":"10.1016/j.prp.2025.156278","DOIUrl":"10.1016/j.prp.2025.156278","url":null,"abstract":"<div><div>Uterine carcinosarcomas (UCS), also known as malignant mixed Müllerian tumors, are rare and aggressive neoplasms characterized by the coexistence of carcinomatous (epithelial) and sarcomatous (mesenchymal) components. PTEN (Phosphatase and Tensin Homolog) mutations, a hallmark of endometrioid-type carcinomas, play a significant role in the pathogenesis and histological presentation of a subset of uterine carcinosarcomas, contributing to their aggressive behavior and poor prognosis. This overview synthesizes the current understanding of PTEN mutations in carcinosarcomas and their implications for clinical management and therapy. A new approach based on morphological, immunohistochemical, and molecular characteristics is proposed.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156278"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145467116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of C-reactive protein in cervical intraepithelial neoplasia/cancer","authors":"Adriana Pedreañez ,&nbsp;Yenddy Carrero ,&nbsp;Renata Vargas ,&nbsp;Juan P.Hernández Fonseca ,&nbsp;Jesús Mosquera","doi":"10.1016/j.prp.2025.156274","DOIUrl":"10.1016/j.prp.2025.156274","url":null,"abstract":"<div><div>Cervical cancer is one of the most common malignancies in women. This pathology originates from the progression of cervical intraepithelial neoplasia (CIN), induced by high-risk human papillomavirus (HPV) infection. During CIN, an inflammatory process characterized by immune system activation and increased levels of C-reactive protein (CRP) occurs. This protein, generally an indicator of inflammatory processes, also has functions that can influence the pathogenesis of several diseases. This review summarizes the current published literature (searched on Pubmed, EMBASE and Web of Science) regarding the factors that affect pathogenesis of cervical intraepithelial neoplasia/cancer mediated by CRP searched up to 2025. This review highlights the events present in CIN/cancer where CRP may be involved. CRP may induce progression of CIN to cervical cancer through its action on its lectin-like receptor oxidized low-density lipoprotein receptor-1 (LOX-1) and influence events involving complement activation, immune system activation, apoptosis induction, oxidative stress, and modulation of HPV biology.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"276 ","pages":"Article 156274"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145364455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Should we subtype gastric intestinal metaplasia in gastric biopsies, a single institution’s experience","authors":"Haibo Wang ,&nbsp;Yu Liu ,&nbsp;Asra Froze ,&nbsp;Zengying Wu ,&nbsp;Jonathan D. Somma ,&nbsp;Zhiyan Fu","doi":"10.1016/j.prp.2025.156189","DOIUrl":"10.1016/j.prp.2025.156189","url":null,"abstract":"<div><div>Gastric intestinal metaplasia (GIM) is considered a risk factor for gastric dysplasia and adenocarcinoma. While surveillance endoscopies are often performed, particularly for incomplete GIM, the clinical value of histologic subtyping (complete, incomplete, or mixed) remains unclear. This study evaluated the progression risk of different GIM subtypes diagnosed through random gastric biopsies and their association with various clinical factors. Archived pathology data from 206 gastric biopsy cases were analyzed, including 52 negative controls, 56 complete GIM, 54 incomplete GIM, and 44 mixed GIM. Histologic slides were reviewed for subtype confirmation and other pathological changes; clinical data were extracted from medical records. Multiple linear regression was conducted for correlation analysis, and Analysis of Variance was used to compare group means. GIM was predominantly located in the antrum. Over a mean follow-up period of 52.2 months, none of the patients, including 12 under mapping surveillance, developed gastric neoplasia. Significant associations were found between <em>Helicobacter pylori</em> (<em>H. pylori</em>) and all types of GIM. <em>H. pylori</em> infection was also significantly associated with the extent of the GIM. Hypertension showed a trend toward significance in correlation with GIM, but no other associations were identified between GIM and demographic or clinical factors such as gender, age, smoking, diabetes mellitus, or hyperlipidemia. Our findings suggest that the routine subtyping GIM in pathology reports may not be necessary, given the lack of progression to any type of neoplasia within the follow-up period. However, the redemonstrated association between <em>H. pylori</em> and GIM emphasizes the importance of eradication therapy.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"275 ","pages":"Article 156189"},"PeriodicalIF":3.2,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144916280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}