Amphiregulin-Deficient Mice Develop Spasmolytic Polypeptide Expressing Metaplasia and Intestinal Metaplasia
نویسندگان
چکیده
منابع مشابه
Heterogeneity in mouse spasmolytic polypeptide-expressing metaplasia lineages identifies markers of metaplastic progression.
OBJECTIVES Spasmolytic polypeptide-expressing metaplasia (SPEM) develops as a preneoplastic lesion in the stomachs of mice and humans after parietal cell loss. To identify the commonalities and differences between phenotypic SPEM lineages, SPEM were studied from three different mouse models of parietal cell loss: with chronic inflammation with Helicobacter felis infection; with acute inflammati...
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IL-10 Plays a Pivotal Role in Tamoxifen-Induced Spasmolytic Polypeptide-Expressing Metaplasia in Gastric Mucosa
Background/Aims Gastric cancer evolves in the pathologic mucosal milieu, and its development is characterized by both the loss of acid-secreting parietal cells and mucosal cell metaplasia, called spasmolytic polypeptide-expressing metaplasia (SPEM). Cytokines, such as interleukin (IL)-10, IL-1β, and IL-6, play a key role in gastric carcinogenesis. However, changes in the cytokine profile of SPE...
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BACKGROUND & AIMS During aging, physiological changes in the stomach result in more tenuous gastric tissue that is less capable of repairing injury, leading to increased susceptibility to chronic ulceration. Spasmolytic polypeptide/trefoil factor 2-expressing metaplasia (SPEM) is known to emerge after parietal cell loss and during Helicobacter pylori infection, however, its role in gastric ulce...
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The development of intestinal-type gastric cancer is preceded by loss of parietal cells (oxyntic atrophy) and the induction of metaplastic cell lineages in the gastric mucosa. For example, mouse models have shown that spasmolytic polypeptide-expressing metaplasia can develop following oxyntic atrophy through transdifferentiation of zymogen-secreting chief cells. Evolution of spasmolytic polypep...
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ژورنال
عنوان ژورنال: Gastroenterology
سال: 2009
ISSN: 0016-5085
DOI: 10.1053/j.gastro.2008.12.037