<i>CDX‐2</i> homeobox gene expression in human gastric carcinoma and precursor lesions

Kim, Hyung-Seok; Lee, Ji-Shin; Freund, Jean–Noël; Min, Kyung-Whan; Lee, Jeong-Soo; Kim, Wan; Juhng, Sang Woo; Park, Chang-Soo

doi:10.1111/j.1440-1746.2005.03933.x

Cited by 35 publications

(31 citation statements)

References 18 publications

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“…12,13 There are a few reports about CDX2 expression in gastric epithelial dysplasia, but the results are conflicting. For instance, Kim et al 15 reported that 73.3% of low-grade adenomas and 85.5% of high-grade adenomas showed CDX2 expression. In their study, a significant reduction in CDX2 expression was also observed in the foci of gastric epithelial dysplasia when compared with the adjacent metaplastic gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…[12][13][14] However, there are scant and conflicting data about CDX2 expression in gastric epithelial dysplasia. [15][16][17] Gastrointestinal epithelia produce site-specific mucins, 18 and the cell differentiation and lineage of various epithelia have been evaluated in various pathologic conditions based on the core mucin protein expression. [19][20][21] In normal gastric mucosa, MUC5AC localizes on the surface/foveolar epithelium, whereas MUC6 is expressed in the mucous cells of the neck zone of oxyntic mucosa and antral glands.…”

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confidence: 99%

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CDX2 expression in the intestinal-type gastric epithelial neoplasia: frequency and significance

et al. 2010

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CDX2 is an intestinal transcription factor responsible for regulating the proliferation and differentiation of intestinal epithelial cells. In gastric adenocarcinoma, CDX2 expression is known to be associated with limited invasiveness and intestinal phenotypes. The aims of this study were to analyze CDX2 expression in a series of well-characterized cases of gastric epithelial dysplasia, based on the morphologic and mucin phenotypes, and also to analyze CDX2 expression along the metaplasia-dysplasia-carcinoma sequence. CDX2 expression was evaluated in 69 cases of gastric epithelial dysplasia, 88 cases of intestinal-type early gastric cancers, and 56 cases of advanced gastric cancers. Increased CDX2 expression was more frequently associated with adenomatous-type gastric epithelial dysplasia (27/31, 87%) compared with foveolar (7/15, 47%) or hybrid (10/23, 44%) types of gastric epithelial dysplasia (P ¼ 0.001). CDX2 expression correlated with an increase in CD10 expression (P ¼ 0.005), and a decrease in MUC5AC expression (P ¼ 0.001) in gastric epithelial dysplasia. CDX2 expression was also gradually decreased from gastric epithelial dysplasia, to early and advanced gastric cancers (present in 64, 40 and 27% of the cases, respectively). A negative correlation was also observed between CDX2 expression and the depth of tumor invasion. Our results indicate that CDX2 expression is associated with specific morphological and mucin phenotypes of gastric epithelial dysplasias, and decreases progressively with the advancing stage of gastric cancers, suggesting a possible tumor suppressor role for CDX2.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

CDX2 expression in the intestinal-type gastric epithelial neoplasia: frequency and significance

et al. 2010

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“…In particular, non-mutated (second) CDH1 allele resulting chiefly from promoter hypermethylation was likely to disintegrate cell adherens junctions and was privy to loss of cell polarity, subsequent to which, β-catenin was activated and HDGC initiated (63,64). Intestinespecific transcription factor CDX2 has been found responding to the generation of gastric adenocarcinoma from intestinal metaplasia, which revealed nuclear staining of β-catenin and APC gene mutations simultaneously (65,66).…”

Section: Wnt/β-catenin Pathway and Gastric Cancermentioning

confidence: 99%

Interaction between Wnt/β-catenin pathway and microRNAs regulates epithelial-mesenchymal transition in gastric cancer (Review)

Zhuang

Jiang

et al. 2016

International Journal of Oncology

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Abstract. Gastric cancer (GC) is the third primary cause of cancer-related mortality and one of the most common type of malignant diseases worldwide. Despite remarkable progress in multimodality therapy, advanced GC with high aggressiveness always ends in treatment failure. Epithelialmesenchymal transition (EMT) has been widely recognized to be a key process associating with GC evolution, during which cancer cells go through phenotypic variations and acquire the capability of migration and invasion. Wnt/β-catenin pathway has established itself as an EMT regulative signaling due to its maintenance of epithelial integrity as well as tight adherens junctions while mutations of its components will lead to GC initiation and diffusion. The E-cadherin/β-catenin complex plays an important role in stabilizing β-catenin at cell membrane while disruption of this compound gives rise to nuclear translocation of β-catenin, which accounts for upregulation of EMT biomarkers and unfavorable prognosis. Additionally, several microRNAs positively or negatively modify EMT by reciprocally acting with certain target genes of Wnt/β-catenin pathway in GC. Thus, this review centers on the strong associations between Wnt/β-catenin pathway and microRNAs during alteration of EMT in GC, which may induce advantageous therapeutic strategies for human gastric cancer.

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“…Indeed, it has been demonstrated that gastric Cdx2 expression alone was sufficient to induce intestinal metaplasia in mice [56] , and long-standing intestinal metaplasia induces invasive GC in CDX2 transgenic mice [57] . In addition, Cdx2 expression was increased in high-grade dysplasia and intestinal-type gastric adenocarcinomas compared to lowgrade dysplasia [58] . Taken together, these findings suggest that Cdx2 expression in GC may contribute to the progression of gastric carcinogenesis and that its activation may represent an early event.…”

Section: Caudal Type Homeobox 2 (Cdx2)mentioning

confidence: 91%

Molecular Pathology of Gastric Carcinoma

Jang

Kim²

2011

Pathobiology

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Gastric carcinoma (GC) is a biologically heterogeneous disease involving numerous genetic and epigenetic alterations. A very small proportion of GCs can be caused by a specific germ-line mutation of the E-cadherin gene (CDH1). Sporadic GC is developed through multistep processes that begin with Helicobacter pylori-induced atrophic gastritis. Epstein-Barr virus is another infectious cause of GC, and the above two infection-associated GCs are characterized by global CpG island methylation in the promoter region of cancer-related genes. Mutations of tumor protein p53 (TP53) and β-catenin (CTNNB1) genes occur early in the development of GC and contribute to gastric carcinogenesis. Furthermore, significant numbers of GCs show loss of Runx3 due to hemizygous deletion and hypermethylation of the promoter region. Aberrant Cdx2 expression has been shown in precancerous lesions as well as GC. However, it remains unclear whether Cdx2 plays an oncogenic role in gastric carcinogenesis. GC with microsatellite instability is also a well-defined subset exhibiting distinctive clinicopathologic features. Targeted therapy against GC with ERBB2 amplification recently improved the prognosis of patients with advanced GC. In addition, epigenetic changes in GC could be attractive targets for cancer treatment with modulators. A genome-wide search has been undertaken to identify novel methylation-silenced genes in GC, which will help us understand the overall molecular features of GC and further provide novel opportunities in the treatment of GC.

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CDX‐2 homeobox gene expression in human gastric carcinoma and precursor lesions

Abstract: These findings suggest that CDX-2 expression in stomach cancer may be a marker of the progression of gastric carcinogenesis, and that its activation may represent an early event.

Cited by 35 publications

References 18 publications

CDX2 expression in the intestinal-type gastric epithelial neoplasia: frequency and significance

CDX2 expression in the intestinal-type gastric epithelial neoplasia: frequency and significance

Interaction between Wnt/β-catenin pathway and microRNAs regulates epithelial-mesenchymal transition in gastric cancer (Review)

Molecular Pathology of Gastric Carcinoma

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