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10.1007/s10120-009-0527-6

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C4502916!4502916!20047123
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suck abstract from ncbi


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pmid20047123      Gastric+Cancer 2009 ; 12 (4): 189-97
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  • Current Understanding of SPEM and its Standing in the Preneoplastic Process #MMPMID20047123
  • Weis VG; Goldenring JR
  • Gastric Cancer 2009[]; 12 (4): 189-97 PMID20047123show ga
  • Gastric cancer is the second leading cause of cancer-related death worldwide, but the details of gastric carcinogenesis remain unclear. In humans, two preneoplastic metaplasias are associated with the pre-cancerous stomach: intestinal metaplasia and Spasmolytic Polypeptide-expressing Metaplasia (SPEM). While mouse models of Helicobacter sp. Infection have not shown intestinal metaplasia, a number of mouse models lead to evolution of SPEM. In this review, we summarize increasing data that indicates that SPEM arises in the setting of parietal cell loss, either following acute drug-induced oxyntic atrophy or in chronic oxyntic atrophy associated with H. felis infection. Importantly, recent investigations support the origin of SPEM through transdifferentiation from mature chief cells following parietal cell loss. Novel biomarkers of SPEM, such as HE4, hold promise as specific markers of the metaplastic process distinct from normal gastric lineages. Staining with HE4 in humans and other studies in gerbils suggest that SPEM arises initially in the human stomach following parietal cell loss and then further evolves into intestinal metaplasia, likely in association with chronic inflammation. Further studies are needed to broaden our knowledge of metaplasia and early cancer-specific biomarkers that could give insights into both lineage derivation and pre-neoplasia detection.
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