121 results match your criteria spem stomachs


WFDC2 Promotes Spasmolytic Polypeptide-Expressing Metaplasia Through the Up-Regulation of IL33 in Response to Injury.

Gastroenterology 2021 Jun 8. Epub 2021 Jun 8.

Severance Biomedical Science Institute, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. Electronic address:

Background & Aims: WAP 4-disulfide core domain protein 2 (WFDC2), also known as human epididymis protein 4, is a small secretory protein that is highly expressed in fibrosis and human cancers, particularly in the ovaries, lungs, and stomach. However, the role of WFDC2 in carcinogenesis is not fully understood. The present study aimed to investigate the role of WFDC2 in gastric carcinogenesis with the use of preneoplastic metaplasia models. Read More

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Glucocorticoids and Androgens Protect From Gastric Metaplasia by Suppressing Group 2 Innate Lymphoid Cell Activation.

Gastroenterology 2021 Aug 7;161(2):637-652.e4. Epub 2021 May 7.

Molecular Endocrinology Group, Signal Transduction Laboratory, North Carolina. Electronic address:

Background & Aims: The immune compartment is critical for maintaining tissue homeostasis. A weak immune response increases susceptibility to infection, but immune hyperactivation causes tissue damage, and chronic inflammation may lead to cancer development. In the stomach, inflammation damages the gastric glands and drives the development of potentially preneoplastic metaplasia. Read More

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Pyloric, pseudopyloric, and spasmolytic polypeptide-expressing metaplasias in autoimmune gastritis: a case series of 22 Japanese patients.

Virchows Arch 2021 Jul 30;479(1):169-178. Epub 2021 Jan 30.

Department of Gastroenterology, Faculty of Medicine, Oita University, Yufu, Oita, Japan.

There are two types of pyloric gland-like metaplasia in the corpus of stomach: pyloric and pseudopyloric metaplasias. They show the same morphology as the original pyloric glands in H&E staining. Pseudopyloric metaplasia is positive for pepsinogen (PG) I immunohistochemically, whereas pyloric metaplasia is negative. Read More

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Interleukin 33 Triggers Early Eosinophil-Dependent Events Leading to Metaplasia in a Chronic Model of Gastritis-Prone Mice.

Gastroenterology 2021 01 1;160(1):302-316.e7. Epub 2020 Oct 1.

Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio. Electronic address:

Background & Aims: Interleukin (IL)33/IL1F11 is an important mediator for the development of type 2 T-helper cell (Th2)-driven inflammatory disorders and has also been implicated in the pathogenesis of gastrointestinal (GI)-related cancers, including gastric carcinoma. We therefore sought to mechanistically determine IL33's potential role as a critical factor linking chronic inflammation and gastric carcinogenesis using gastritis-prone SAMP1/YitFc (SAMP) mice.

Methods: SAMP and (parental control) AKR mice were assessed for baseline gastritis and progression to metaplasia. Read More

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January 2021

DDIT4 Licenses Only Healthy Cells to Proliferate During Injury-induced Metaplasia.

Gastroenterology 2021 01 19;160(1):260-271.e10. Epub 2020 Sep 19.

Division of Gastroenterology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri; Department of Developmental Biology, Washington University School of Medicine, St Louis, Missouri. Electronic address:

Background And Aims: In stomach, metaplasia can arise from differentiated chief cells that become mitotic via paligenosis, a stepwise program. In paligenosis, mitosis initiation requires reactivation of the cellular energy hub mTORC1 after initial mTORC1 suppression by DNA damage induced transcript 4 (DDIT4 aka REDD1). Here, we use DDIT4-deficient mice and human cells to study how metaplasia increases tumorigenesis risk. Read More

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January 2021

Group 2 Innate Lymphoid Cells Coordinate Damage Response in the Stomach.

Gastroenterology 2020 12 4;159(6):2077-2091.e8. Epub 2020 Sep 4.

Department of Cell and Developmental Biology, Nashville, Tennessee; Epithelial Biology Center, Nashville, Tennessee; Section of Surgical Sciences, Nashville, Tennessee; Nashville VA Medical Center, Nashville, Tennessee. Electronic address:

Background & Aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and foveolar cell hyperplasia. Acute gastric damage elicits a type-2 inflammatory response that includes production of type-2 cytokines and infiltration by eosinophils and alternatively activated macrophages. Stomachs of mice that lack interleukin 33 (IL33) or interleukin 13 (IL13) did not undergo epithelial reprogramming after drug-induced injury. Read More

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December 2020

Single-Cell Transcriptional Analyses Identify Lineage-Specific Epithelial Responses to Inflammation and Metaplastic Development in the Gastric Corpus.

Gastroenterology 2020 12 21;159(6):2116-2129.e4. Epub 2020 Aug 21.

Department of Molecular Microbiology & Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri. Electronic address:

Background & Aims: Chronic atrophic gastritis can lead to gastric metaplasia and increase risk of gastric adenocarcinoma. Metaplasia is a precancerous lesion associated with an increased risk for carcinogenesis, but the mechanism(s) by which inflammation induces metaplasia are poorly understood. We investigated transcriptional programs in mucous neck cells and chief cells as they progress to metaplasia mice with chronic gastritis. Read More

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December 2020

Role of metaplasia during gastric regeneration.

Am J Physiol Cell Physiol 2020 12 5;319(6):C947-C954. Epub 2020 Aug 5.

Department of Cellular and Molecular Medicine, University of Arizona College of Medicine, Tucson, Arizona.

Spasmolytic polypeptide/trefoil factor 2 (TFF2)-expressing metaplasia (SPEM) is a mucous-secreting reparative lineage that emerges at the ulcer margin in response to gastric injury. Under conditions of chronic inflammation with parietal cell loss, SPEM has been found to emerge and evolve into neoplasia. Cluster-of-differentiation gene 44 (CD44) is known to coordinate normal and metaplastic epithelial cell proliferation. Read More

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December 2020

Development of Pancreatic Acinar Cell Metaplasia During Gastric Repair in a Rat Duodenal Contents Reflux Model.

Dig Dis Sci 2021 Apr 21;66(4):1072-1079. Epub 2020 May 21.

Division of Diagnostic Pathology, Shiga University of Medical Science Hospital, Otsu, Japan.

Background: We previously reported the development of pancreatic acinar cell metaplasia (PACM) in the glandular stomach of a duodenal contents reflux model (reflux model).

Aims: We aimed to investigate the characteristics and histogenesis of PACM using a reflux model.

Methods: A reflux model was created using 8-week-old male Wistar rats, which were killed up to 30 weeks postoperatively. Read More

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Trop2 is upregulated in the transition to dysplasia in the metaplastic gastric mucosa.

J Pathol 2020 07 15;251(3):336-347. Epub 2020 Jun 15.

Department of Surgery, Vanderbilt University School of Medicine, Nashville, TN, USA.

Intestinal-type gastric adenocarcinoma arises in a field of pre-existing metaplasia. While biomarkers of cancer and metaplasia have been identified, the definition of dysplastic transition as a critical point in the evolution of cancer has remained obscure. We have evaluated Trop2 as a putative marker of the transition from metaplasia to dysplasia in the stomach in multiple mouse models of metaplasia induction and progression. Read More

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Interleukin 27 Protects From Gastric Atrophy and Metaplasia During Chronic Autoimmune Gastritis.

Cell Mol Gastroenterol Hepatol 2020 4;10(3):561-579. Epub 2020 May 4.

Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri. Electronic address:

Background & Aims: The association between chronic inflammation and gastric carcinogenesis is well established, but it is not clear how immune cells and cytokines regulate this process. We investigated the role of interleukin 27 (IL27) in the development of gastric atrophy, hyperplasia, and metaplasia (preneoplastic lesions associated with inflammation-induced gastric cancer) in mice with autoimmune gastritis.

Methods: We performed studies with TxA23 mice (control mice), which express a T-cell receptor against the H+/K+ adenosine triphosphatase α chain and develop autoimmune gastritis, and TxA23xEbi3 mice, which develop gastritis but do not express IL27. Read More

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Histological changes associated with pyloric and pseudopyloric metaplasia after Helicobacter pylori eradication.

Virchows Arch 2020 Oct 30;477(4):489-496. Epub 2020 Apr 30.

Department of Gastroenterology, Faculty of Medicine, Oita University, Yufu, Oita, 879-5593, Japan.

Pyloric metaplasia (PM) and pseudopyloric metaplasia (PPM) are metaplastic changes resulting in pyloric-type glands in the gastric oxyntic mucosa that mainly occur in chronic gastritis caused by Helicobacter pylori (H. pylori) infection. Focusing on PM and PPM, we classified the histological changes in gastric mucosa according to the Updated Sydney System, using 314 biopsy specimens of gastric greater curvature of the middle body before H. Read More

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October 2020

An LCM-based genomic analysis of SPEM, Gastric Cancer and Pyloric Gland Adenoma in an Asian cohort.

Mod Pathol 2020 10 8;33(10):2075-2086. Epub 2020 Apr 8.

Department of Pathology, National University Hospital, Singapore, 119228, Singapore.

Spasmolytic polypeptide-expressing metaplasia (SPEM) and pyloric gland adenoma (PGA) in the stomach are metaplastic and neoplastic lesions, respectively, in which gastric body glands are replaced by pyloric glands. The aim of this study was to evaluate the genomic profile of SPEM and compare it with intestinal-type gastric cancer (GC) and PGA. Thirteen gastrectomies showing PGA with or without dysplasia, GC and SPEM were retrospectively selected. Read More

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October 2020

A Metformin-Responsive Metabolic Pathway Controls Distinct Steps in Gastric Progenitor Fate Decisions and Maturation.

Cell Stem Cell 2020 06 2;26(6):910-925.e6. Epub 2020 Apr 2.

Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA; Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO, USA. Electronic address:

Cellular metabolism plays important functions in dictating stem cell behaviors, although its role in stomach epithelial homeostasis has not been evaluated in depth. Here, we show that the energy sensor AMP kinase (AMPK) governs gastric epithelial progenitor differentiation. Administering the AMPK activator metformin decreases epithelial progenitor proliferation and increases acid-secreting parietal cells (PCs) in mice and organoids. Read More

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microRNA-30a arbitrates intestinal-type early gastric carcinogenesis by directly targeting ITGA2.

Gastric Cancer 2020 07 28;23(4):600-613. Epub 2020 Feb 28.

Cancer Research Institute, Seoul National University College of Medicine, 101 Daehak-Ro, Jongno-gu, Seoul, 03080, South Korea.

Background: Spasmolytic polypeptide-expressing metaplasia (SPEM) is considered a precursor lesion of intestinal metaplasia and intestinal-type gastric cancer (GC), but little is known about microRNA alterations during metaplasia and GC developments. Here, we investigate miR-30a expression in gastric lesions and identify its novel target gene which is associated with the intestinal-type GC.

Methods: We conducted in situ hybridization and qRT-PCR to determine miR-30a expression in gastric tissues. Read More

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Deoxycholic acid-stimulated macrophage-derived exosomes promote spasmolytic polypeptide-expressing metaplasia in the stomach.

Biochem Biophys Res Commun 2020 04 4;524(3):649-655. Epub 2020 Feb 4.

Department of Gastroenterology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Pancreatic Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Gastroenterology, Shanghai General Hospital, Nanjing Medical University, Nanjing, China. Electronic address:

Rationale: Spasmolytic polypeptide-expressing metaplasia (SPEM) is an important risk factor for the occurrence of gastric cancer. It may be driven by a chronic inflammatory environment in which macrophage is involved. Studies have shown that intestinal metaplasia may originate from SPEM, and bile acid-induced chronic inflammation plays an important role in the process of intestinal metaplasia. Read More

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GPR30-Expressing Gastric Chief Cells Do Not Dedifferentiate But Are Eliminated via PDK-Dependent Cell Competition During Development of Metaplasia.

Gastroenterology 2020 05 4;158(6):1650-1666.e15. Epub 2020 Feb 4.

Department of Gastroenterology, Graduate school of Medicine, the University of Tokyo, Tokyo, Japan.

Background & Aims: Gastric chief cells, a mature cell type that secretes digestive enzymes, have been proposed to be the origin of metaplasia and cancer through dedifferentiation or transdifferentiation. However, studies supporting this claim have had technical limitations, including issues with the specificity of chief cell markers and the toxicity of drugs used. We therefore sought to identify genes expressed specifically in chief cells and establish a model to trace these cells. Read More

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Gastric Corpus Mucosal Hyperplasia and Neuroendocrine Cell Hyperplasia, but not Spasmolytic Polypeptide-Expressing Metaplasia, Is Prevented by a Gastrin Receptor Antagonist in H/KATPase Beta Subunit Knockout Mice.

Int J Mol Sci 2020 Jan 31;21(3). Epub 2020 Jan 31.

Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, NTNU-Norwegian University of Science and Technology, 7491 Trondheim, Norway.

Proton pump inhibitor use is associated with an increased risk of gastric cancer, which may be mediated by hypergastrinemia. Spasmolytic polypeptide-expression metaplasia (SPEM) has been proposed as a precursor of gastric cancer. We have examined the effects of the gastrin receptor antagonist netazepide (NTZ) or vehicle on the gastric corpus mucosa of H/KATPase beta subunit knockout (KO) and wild-type (WT) mice. Read More

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January 2020

MiR130b from Schlafen4 MDSCs stimulates epithelial proliferation and correlates with preneoplastic changes prior to gastric cancer.

Gut 2020 10 24;69(10):1750-1761. Epub 2020 Jan 24.

Internal Medicine-Gastroenterology, University of Michigan, Ann Arbor, Michigan, USA

The myeloid differentiation factor Schlafen4 (Slfn4) marks a subset of myeloid-derived suppressor cells (MDSCs) in the stomach during -induced spasmolytic polypeptide-expressing metaplasia (SPEM).

Objective: To identify the gene products expressed by Slfn4-MDSCs and to determine how they promote SPEM.

Design: We performed transcriptome analyses for both coding genes (mRNA by RNA-Seq) and non-coding genes (microRNAs using NanoString nCounter) using flow-sorted SLFN4 and SLFN4 cells from -infected mice exhibiting metaplasia at 6 months postinfection. Read More

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October 2020

Proliferation and Differentiation of Gastric Mucous Neck and Chief Cells During Homeostasis and Injury-induced Metaplasia.

Gastroenterology 2020 02 5;158(3):598-609.e5. Epub 2019 Oct 5.

Division of Gastroenterology, Department of Medicine, Washington University School of Medicine, St Louis, Missouri; Department of Developmental Biology, Washington University School of Medicine, St Louis, Missouri; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri. Electronic address:

Background & Aims: Adult zymogen-producing (zymogenic) chief cells (ZCs) in the mammalian gastric gland base are believed to arise from descending mucous neck cells, which arise from stem cells. Gastric injury, such as from Helicobacter pylori infection in patients with chronic atrophic gastritis, can cause metaplasia, characterized by gastric cell expression of markers of wound-healing; these cells are called spasmolytic polypeptide-expressing metaplasia (SPEM) cells. We investigated differentiation and proliferation patterns of neck cells, ZCs, and SPEM cells in mice. Read More

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February 2020

Single-cell transcriptional analyses of spasmolytic polypeptide-expressing metaplasia arising from acute drug injury and chronic inflammation in the stomach.

Gut 2020 06 3;69(6):1027-1038. Epub 2019 Sep 3.

Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, Missouri, USA

Objective: Spasmolytic polypeptide-expressing metaplasia (SPEM) is a regenerative lesion in the gastric mucosa and is a potential precursor to intestinal metaplasia/gastric adenocarcinoma in a chronic inflammatory setting. The goal of these studies was to define the transcriptional changes associated with SPEM at the individual cell level in response to acute drug injury and chronic inflammatory damage in the gastric mucosa.

Design: Epithelial cells were isolated from the gastric corpus of healthy stomachs and stomachs with drug-induced and inflammation-induced SPEM lesions. Read More

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Decrease in MiR-148a Expression During Initiation of Chief Cell Transdifferentiation.

Cell Mol Gastroenterol Hepatol 2020 29;9(1):61-78. Epub 2019 Aug 29.

Nashville VA Medical Center, Nashville, Tennessee; Department of Surgery, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Department of Cell and Developmental Biology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Epithelial Biology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee. Electronic address:

Gastric chief cells differentiate from mucous neck cells and develop their mature state at the base of oxyntic glands with expression of secretory zymogen granules. After parietal cell loss, chief cells transdifferentiate into mucous cell metaplasia, designated spasmolytic polypeptide-expressing metaplasia (SPEM), which is considered a candidate precursor of gastric cancer. We examined the range of microRNA (miRNA) expression in chief cells and identified miRNAs involved in chief cell transdifferentiation into SPEM. Read More

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Diagnosis: gastric intestinal metaplasia - what to do next?

Curr Opin Gastroenterol 2019 11;35(6):535-543

Department of Medicine, Michael E. DeBakey VA Medical Center, Baylor College of Medicine Houston, Texas, USA.

Purpose Of Review: One of the most vexing problems for gastroenterologists is what actions to take after receiving a histological diagnosis of gastric intestinal metaplasia. We approach the problem by starting with suggesting a biopsy protocol that ensures obtaining the biopsies required for diagnosis, assessing the status of the gastric mucosa, and effective communication with the pathologist and patient.

Recent Findings: The rediscovery and integration of the long history of gastric damage and repair resulting in pseudopyloric metaplasia (called SPEM) into the thinking of investigators working with animal models of gastric cancer has resulted in improved ability to separate changes associated with benign repair from those associated with inflammation-associated gastric carcinogenesis. Read More

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November 2019

Muc5ac null mice are predisposed to spontaneous gastric antro-pyloric hyperplasia and adenomas coupled with attenuated H. pylori-induced corpus mucous metaplasia.

Lab Invest 2019 12 9;99(12):1887-1905. Epub 2019 Aug 9.

Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.

Gastric cancer (GC) is the third leading cause of cancer-related deaths worldwide and is strongly associated with chronic Helicobacter pylori (Hp) infection. The ability of Hp to closely adhere to the gastric surface protective mucous layer containing mucins (MUC in humans and Muc in animals), primarily Muc5ac, is integral in the stepwise pathogenesis from gastritis to cancer. To probe the role of Muc5ac in Hp-induced gastric pathology, Muc5ac and Muc5ac (WT) mice were experimentally infected with Hp Sydney strain (SS1). Read More

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December 2019

Cystine/Glutamate Antiporter (xCT) Is Required for Chief Cell Plasticity After Gastric Injury.

Cell Mol Gastroenterol Hepatol 2019 6;8(3):379-405. Epub 2019 May 6.

Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, Tennessee; Epithelial Biology Center, Vanderbilt University School of Medicine, Nashville, Tennessee; Section of Surgical Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee; Nashville Veterans Affairs Medical Center, Vanderbilt University School of Medicine, Nashville, Tennessee. Electronic address:

Background & Aims: Many differentiated epithelial cell types are able to reprogram in response to tissue damage. Although reprogramming represents an important physiological response to injury, the regulation of cellular plasticity is not well understood. Damage to the gastric epithelium initiates reprogramming of zymogenic chief cells into a metaplastic cell lineage known as spasmolytic polypeptide-expressing metaplasia (SPEM). Read More

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Spasmolytic polypeptide-expressing metaplasia associated with higher expressions of miR-21, 155, and 223 can be regressed by Helicobacter pylori eradication in the gastric cancer familial relatives.

Helicobacter 2019 Jun 16;24(3):e12578. Epub 2019 Apr 16.

Institute of Clinical Medicine, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.

Background And Aims: Spasmolytic polypeptide-expressing metaplasia (SPEM) is a preneoplastic gastric cancer lesion related to epigenetic microRNA (miRNA) expression. This study elucidated whether Helicobacter pylori-infected first-degree relatives of patients with gastric cancer (GCF) are susceptible to have SPEM and correlated with miR-21, 155, and 223 expressions. We also validated whether SPEM and these miRNAs can be regressed after H pylori eradication. Read More

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Deficiency of Stomach-Type Claudin-18 in Mice Induces Gastric Tumor Formation Independent of H pylori Infection.

Cell Mol Gastroenterol Hepatol 2019 23;8(1):119-142. Epub 2019 Mar 23.

Laboratory of Biological Science, Graduate School of Frontier Biosciences, and Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address:

Background & Aims: Epithelial cells are joined by tight junctions (TJs) to form a cell sheet. In the stomach, epithelial cell sheet forms an essential barrier against gastric material, including gastric acid. Although the decreased expression of stomach-type claudin-18 (stCldn18), a TJ protein, is generally observed in human gastritis and gastric cancer, its pathological roles are not fully understood. Read More

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Evidence for heightened genetic instability in precancerous spasmolytic polypeptide expressing gastric glands.

J Med Genet 2020 06 15;57(6):385-388. Epub 2019 Mar 15.

Bio-ID Center, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.

Background: Spasmolytic polypeptide-expressing metaplasia (SPEM) is present in more than 90% of resected gastric cancer tissues. However, although widely regarded as a pre-cancerous tissue, its genetic characteristics have not been well studied.

Methods: Immunohistochemistry using Trefoil factor 2 (TFF2) antibodies was used to identify TFF2-positive SPEM cells within SPEM glands in the stomach of -infected mice and human clinical samples. Read More

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Endogenous glucocorticoids prevent gastric metaplasia by suppressing spontaneous inflammation.

J Clin Invest 2019 03 18;129(3):1345-1358. Epub 2019 Feb 18.

Molecular Endocrinology Group, Signal Transduction Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.

In the stomach, chronic inflammation causes metaplasia and creates a favorable environment for the evolution of gastric cancer. Glucocorticoids are steroid hormones that repress proinflammatory stimuli, but their role in the stomach is unknown. In this study, we show that endogenous glucocorticoids are required to maintain gastric homeostasis. Read More

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Interferon-γ directly induces gastric epithelial cell death and is required for progression to metaplasia.

J Pathol 2019 04 24;247(4):513-523. Epub 2019 Jan 24.

Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri, USA.

Chronic inflammation of the gastric mucosa, often caused by autoimmune gastritis and/or infection with Helicobacter pylori, can lead to atrophy of acid-secreting parietal cells with metaplasia of remaining cells. The histological pattern marks a critical step in the progression from chronic gastritis to gastric cancer, yet underlying mechanism(s) of inflammation-induced cell death of gastric epithelial cells are poorly understood. We investigated direct effects of a type 1 cytokine associated with autoimmunity and infection, interferon-γ (IFN-γ), on gastric epithelial cells. Read More

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