Guilt by association: intestinal metaplasia does not progress to gastric cancer.
Guilt by association: intestinal metaplasia does not progress to gastric cancer.
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DOI：
10.1097/mog.0000000000000472
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发表时间：
2018-11
影响因子：
2.5
通讯作者：
Zou WY
中科院分区：
文献类型：
--
作者：
Graham DY;Zou WY
本文就胃癌与肠上皮化生/假幽门上皮化生（SPEM）关系的新认识作一综述。我们讨论最近的研究是否关闭或扩大了关于小鼠或人类胃癌发病机制的知识差距。最近在小鼠模型中的研究为导致胃癌的事件的细胞起源和进展提供了各种新的见解。许多人认为肠化生/假幽门化生/SPEM直接转化为胃癌。然而，来自不同研究者和模型的结果是相互矛盾的，并且经常描述人类研究中不存在的事件。幽门螺杆菌相关性胃炎和自身免疫性胃炎均可引起胃萎缩伴广泛肠上皮化生和胃微生物组异常。但只有H.幽门螺杆菌胃炎有腺癌的风险。小鼠模型报告的差异可以最好地解释为不同的再生和修复模型的结果，而不是胃癌模型。总的来说，这些数据仍然与最初的假设一致，即胃癌是由胃干细胞遗传不稳定性增加引起的，而不是由化生直接转变为癌症。肠上皮化生、假幽门化生和SPEM都被错误地指控为有罪的基础上协会。
This review integrates the new thinking about relationships between gastric cancer and intestinal metaplasia/pseudopyloric metaplasia (SPEM). We address whether recent studies have closed or widened the knowledge gap regarding gastric cancer pathogenesis in mice or humans. Recent studies in mouse models have provided a variety of new insights into the cellular origin and progression of events resulting in gastric cancer. Many suggest a direct transformation from intestinal metaplasia/pseudopyloric metaplasia/SPEM to gastric cancer. However, results from different investigator and models are conflicting and often describe events not present in studies in humans. Both Helicobacter pylori-associated and autoimmune gastritis may produce gastric atrophy with extensive intestinal metaplasia and an abnormal gastric microbiome. However, only H. pylori gastritis carries a risk for adenocarcinoma. The differences reported with mouse models can best be explained as the results of different models of regeneration and repair rather than as models of gastric cancer. Overall, the data remains consistent with the original hypothesis that gastric cancer results from increased genetic instability of gastric stem cells rather than a direct transition from metaplasia to cancer. Intestinal metaplasia, pseudopyloric metaplasia, and SPEM have all been falsely accused based on guilt by association.