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Histopathology and molecular pathology of intestinal metaplasia

机译：肠化生的组织病理学和分子病理学

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The pathogenesis of intestinal metaplasia (IM) of the human stomach remains completely unknown. Several classifications of IM have been suggested. Recent investigators have examined epithelial cell phenotypes in IM through immunohistochemistry, and revealed that gastric IM glands consist of a mixture of gastric and intestinal cell phenotypes. This implies that a heterogeneous cell population with both gastric and intestinal phenotypes would develop into a single intestinal phenotype. Recently, an intestinal stem cell marker was found to be present in the putative position of human gastric glands, whereas it was absent in gastric IM glands. This supports the assumption that IM is a consequence of abnormal stem cell differentiation, leading to lack of differentiation into any of the normal intestinal epithelial phenotypes. Recent advances in molecular biology have revealed intestinal transcriptional factors (Cdx1/Cdx2), suggesting that upregulation of Cdx2 may trigger the initiation and development of IMin the stomach. Epidemiological evidence indicates that Helicobacter pylori is a major cause of IM but might not be solely responsible for its induction. A variation in host and bacterial background that predisposes to the development of IM has been revealed.
机译：人胃肠上皮化生（IM）的发病机制仍然完全未知。已经提出IM的几种分类。最近的研究者已经通过免疫组织化学检查了IM中的上皮细胞表型，并发现胃IM腺体由胃和肠细胞表型的混合物组成。这意味着具有胃和肠表型的异质细胞群将发展成单个肠表型。最近，发现在人胃腺的推定位置存在肠道干细胞标记，而在胃IM腺中则不存在。这支持了IM是干细胞异常分化的结果的假设，导致干细胞缺乏向任何正常肠道上皮表型的分化。分子生物学的最新进展揭示了肠道转录因子（Cdx1 / Cdx2），这表明Cdx2的上调可能触发了IM在胃中的启动和发展。流行病学证据表明，幽门螺杆菌是IM的主要病因，但可能并非完全由IM引起。已经揭示了宿主和细菌背景的变异，这容易导致IM的发展。

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