Biology of intestinal metaplasia in 2008:: More than a simple phenotypic alteration

被引：40

作者：

Gutierrez-Gonzalez, L. ^{[1
,3
,4
]}

Wright, N. A. ^{[1
,2
]}

机构：

[1] London Res Inst, Can Res UK, Histopathol Unit, London WC2A 3PX, England

[2] Barts & London Queen Marys Sch Med & Dent, London, England

[3] CIBERehd, Inst Hlth Sci Aragon, Zaragoza, Spain

[4] Inst Hlth Sci Carlos III, Madrid, Spain

来源：

DIGESTIVE AND LIVER DISEASE | 2008年 / 40卷 / 07期

关键词：

intestinal metaplasia; monoclonal conversion; SPEM; trefoil factor family;

D O I：

10.1016/j.dld.2008.02.029

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

This review concentrates on one main aspect of cancerization in the oesophagus and stomach: principally, intestinal metaplasia. There are at least two other important pathways that lead to cancer and do not need such a morphological transformation. One is the gastric type of carcinoma on the Lauren classification, which arises directly from the stem cell zone and is the signet ring form of cancer, while the other is spasmolytic polypeptide-expressing metaplasia (SPEM)-spasmolytic polypeptide (TFF2) expressing metaplasia, where the gastric glands become filled with TFF2-expressing cells and may also lead to gastric dysplasia and cancer. The development of intestinal metaplasia is complex. Here, we examine intestinal metaplasia in molecular terms, noting the over-expression of Cdx1, Cdx2, Pdx1, Oct1, TFF3 and the downregulation of Hedgehog signalling; Runx3 is deactivated by epigenetic silencing, and pathways such as Wnt and MARK/ERK are involved. These changes start to explain the principles of the development of intestinal metaplasia and suggest that the regulation of these genes is of importance in the development of gastric cancer. (c) 2008 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

引用

页码：510 / 522

页数：13

共 160 条

[1] OCT-1 is over-expressed in intestinal metaplasia and intestinal gastric carcinomas and binds to, but does not transactivate, CDX2 in gastric cells [J].