Abstract
This chapter discusses the role of immunohistochemical (IHC) expression of beta-catenin and mucin in stomach cancer. Beta-catenin plays an important role in the cell-cell adhesion system and in the wingless/wnt cell-cell signalling system. Beta-catenin acts as E-cadherin binding protein mostly on the cell membrane. Abnormally accumulated beta-catenin causes cell proliferation and carcinogenesis. Intracellular levels of beta-catenin are mainly regulated by degradation that is probably initiated, by interaction, with the adenomatous polyposis coli (APC) protein and glycogen synthase kinase (GSK)-3 beta. Abnormality in exon3 of the beta-catenin gene result in accumulation of beta-catenin or phosphorylation of these residues may inhibit degradation. Beta-catenin mutations and expression are analyzed in various common cancers. The relationship between beta-catenin expression and phenotype of group C lesion is analyzed. Mutations of the APC gene occur and are detected during the early stages of gastric adenoma development. The beta-catenin expression does not always reflect the malignant transformation in the early stage of gastric tumorigenesis and beta-catenin abnormality is only one particular aspect of malignant transformation.
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