ArticleLaboratory investigation; a journal of technical methods and pathology2012
Gastric tumor development in Smad3-deficient mice initiates from forestomach/glandular transition zone along the lesser curvature.
Article in Laboratory investigation; a journal of technical methods and pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Global research trends in signaling pathways of spasmolytic polypeptide-expressing metaplasia pathogenesis: a bibliometric analysis.Frontiers in oncology · 2025Pooled it
- GDF9, NPHS1, and RET Mark Gastric Neuroendocrine Cells and Their Disruption in a PKA-Driven Gastric Preneoplasia Model.International journal of molecular sciences · 2026Article
- Microenvironmental stiffness directs microtubule perturbation in chondrocyte mitosis via ILK-refilinB/Smad3 axis.Bone research · 2026Article
- The Changing Landscape of Hereditary Diffuse Gastric Cancer.Journal of gastric cancer · 2026Review
- Precancerous pathways to gastric cancer: a review of experimental animal models recapitulating the correa cascade.Frontiers in cell and developmental biology · 2025Review
- Dynamic tuft cell expansion during gastric metaplasia and dysplasia.The journal of pathology. Clinical research · 2024Article
- The Physiology of the Gastric Parietal Cell.Physiological reviews · 2020Review
- BMP Signaling in Development, Stem Cells, and Diseases of the Gastrointestinal Tract.Annual review of physiology · 2020Review
- Gastric Leptin and Tumorigenesis: Beyond Obesity.International journal of molecular sciences · 2019Review
- Pancreatic DCLK1Cancer letters · 2018Article
- Acid and the basis for cellular plasticity and reprogramming in gastric repair and cancer.Nature reviews. Gastroenterology & hepatology · 2018Review
- Metaplasia in the Stomach-Precursor of Gastric Cancer?International journal of molecular sciences · 2017Review
- A Summary of the 2016 James W. Freston Conference of the American Gastroenterological Association: Intestinal Metaplasia in the Esophagus and Stomach: Origins, Differences, Similarities and Significance.Gastroenterology · 2017Article
- Regulation of Gastric Carcinogenesis by Inflammatory Cytokines.Cellular and molecular gastroenterology and hepatology · 2017Review
- Article
- Murine Models of Gastric Corpus Preneoplasia.Cellular and molecular gastroenterology and hepatology · 2017Review
- Unique Cellular Lineage Composition of the First Gland of the Mouse Gastric Corpus.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Mouse models for gastric cancer: Matching models to biological questions.Journal of gastroenterology and hepatology · 2016Review
- Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.Advances in experimental medicine and biology · 2016Review
- Clinicopathological characterisation of small (2 cm or less) proximal and distal gastric carcinomas in a Chinese population.Pathology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
SMAD proteins are downstream effectors of the TGF-β signaling pathway. Smad3-null mice develop colorectal cancer by 6 months of age. In this study, we have examined whether the loss of Smad3 promotes gastric neoplasia in mice. The stomachs of Smad3⁻/⁻ mice were compared with age-matched Smad3 heterozygous and wild-type mice. E-cadherin, Ki-67, phosphoSTAT3, and TFF2/SP expression was analyzed by immunohistochemisty. The short hairpin RNA (ShRNA)-mediated knockdown of Smad3 in AGS and MKN28 cells was also performed. In addition, we examined alterations in DCLK1-expressing cells. Smad3⁻/⁻ mouse stomachs at 6 months of age revealed the presence of exophytic growths along the lesser curvature in the proximal fundus. Six-month-old Smad3⁻/⁻ mouse stomachs showed metaplastic columnar glands initiating from the transition zone junction between the forestomach and the glandular epithelium along the lesser curvature. Ten-month-old Smad3⁻/⁻ mice all exhibited invasive gastric neoplastic changes with increased Ki-67, phosphoSTAT3 expression, and aberrant cytosolic E-cadherin staining in papillary glands within the invading submucosal gland. The shRNA-mediated knockdown of Smad3 in AGS and MKN28 cells promoted the expression of phosphoSTAT3. DCLK1-expressing cells, which also stained for the tuft cell marker acetylated-α-tubulin, were observed in 10-month-old Smad3⁻/⁻ mice within tumors and in fundic invasive lesions. In conclusion, Smad3-null mice develop gastric tumors in the fundus, which arise from the junction between the forestomach and the glandular epithelium and progress to prominent invasive tumors over time. Smad3-null mice represent a novel model of fundic gastric tumor initiated from forestomach/glandular transition zone along the lesser curvature.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.