Beta-Catenin Expression in Intramucosal Neoplastic Lesions of the Stomach

Abstract

Objective: To clarify roles of beta-catenin in the early stage of gastric tumorigenesis, we investigate beta-catenin expression in stomach intramucosal neoplasms. Methods: For immunohistochemistry, 84 gland-forming neoplasms and 17 signet-ring cell carcinomas were examined. The gland-forming neoplasms were grouped according to the Vienna classification: group A (low-grade adenoma/dysplasia), group B (high-grade adenoma/dysplasia) and group C (intramucosal carcinoma). Results: Strong nuclear expression was detected not only in group C (21.4%) but in groups A (20.8%) and B (11.2%). Strong cytoplasmic expression was detected in groups A, B and C: 16.7, 11.2 and 16.7%, respectively. Loss of membranous stainings (LOM) were also detected in groups A, B and C: 20.8, 22.2 and 31.0%, respectively. No significant difference was found among groups A, B and C with respect to nuclear, cytoplasmic, and membranous expression. Regarding signet-ring cell carcinomas, all cases were essentially negative for nuclear expression and 11.8% of the cases showed weak cytoplasmic expression as well as LOM. There were obvious differences between gland-forming adenocarcinoma and signet-ring cell carcinoma with respect to nuclear and cytoplasmic expression but not in terms of membranous expression. Conclusion: These findings suggest that beta-catenin expression does not always reflect the malignant transformations in the early stage of gastric tumorigenesis.

The expression of E-cadherin-catenin complex in patients with advanced gastric cancer: role in formation of metastasis.

“…However, according to other researchers no correlation can be found between E-cadherin or β-catenin expression and the invasion depth [27]. What is more, neither nuclear nor cytoplasmatic expression was found in the deep gastric wall referred to as the invasion front [32]. This is in agreement with the finding reported by Miyazawa et al [33] that the nuclear β-catenin expression becomes reduced in correlation with depth of invasion.…”

Helicobacter pyloritargets cancer-associated apical-junctional constituents in gastroids and gastric epithelial cells

“…9 These events lead to β-catenin nuclear accumulation, resulting in transcription of genes implicated in carcinogenesis. Increased β-catenin expression as well as mutations within APC are present in gastric adenocarcinoma specimens, 32 and nuclear accumulation of β-catenin is increased within gastric adenomas and foci of dysplasia, 33–36 suggesting that aberrant activation of β-catenin precedes the development of gastric cancer. Since β-catenin is overexpressed within H. pylori -associated premalignant and malignant lesions, and regulates the transcription of genes that have been implicated in tumour initiation, it is likely that β-catenin is a central component in regulation of epithelial responses to H. pylori that may directly promote tumourigenesis.…”

Gastric Microbiome and Gastric Cancer

“…Non-phosphorylated β-catenin then is able to translocate into the nucleus and direct the transcription of target genes involved in carcinogenesis. β-catenin is over-expressed or APC is mutated in 50% of gastric adenocarcinoma samples, and its localization in the nucleus is increased in gastric adenomas and areas of dysplasia 37 , suggesting aberrant activation of β-catenin is a prerequisite step in the development of stomach cancer. H. pylori induces expression of β-catenin target genes in stomach mucosal tissue in vitro and in co-cultures with gastric epithelial cells, providing support for the possibility that activation of β-catenin is an important event in which H. pylori initiates carcinogenesis.…”