Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.
Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.
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DOI：
10.1007/978-3-319-41388-4_22
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发表时间：
2016
影响因子：
--
通讯作者：
Merchant JL
中科院分区：
文献类型：
--
作者：
Ding L;El Zaatari M;Merchant JL
传统上，Correa范式将胃癌定义为始于慢性炎症的连续病理事件的进展。幽门螺杆菌（Helicobacter pylori，H.幽门螺杆菌）是为什么胃变得慢性发炎的典型解释。急性胃炎症然后导致慢性胃炎、萎缩（特别是泌酸壁细胞的萎缩）、由于粘液颈细胞从酶原细胞的转分化到发育不良的扩张而引起的化生以及最终的癌。本章概述了胃的解剖学和生理学，为在胃肿瘤发生中发挥作用的信号通路奠定基础。最后，主要的已知小鼠模型的胃转化批评的基本原理背后的一代和贡献，我们了解人类癌症亚型。
Gastric cancer has been traditionally defined by the Correa paradigm as a progression of sequential pathological events that begins with chronic inflammation. Infection with Helicobacter pylori (H. pylori) is the typical explanation for why the stomach becomes chronically inflamed. Acute gastric inflammation then leads to chronic gastritis, atrophy particularly of acid-secreting parietal cells, metaplasia due to mucous neck cell expansion from trans-differentiation of zymogenic cells to dysplasia and eventually carcinoma. The chapter contains an overview of gastric anatomy and physiology to set the stage for signaling pathways that play a role in gastric tumorigenesis. Finally, the major known mouse models of gastric transformation are critiqued in terms of the rationale behind their generation and contribution to our understanding of human cancer subtypes.