Journal Article

Increased β-catenin mRNA levels and mutational alterations of the <i>APC</i> and β-catenin gene are present in intestinal-type gastric cancer

Matthias P.A. Ebert, Guo Fei, Sabine Kahmann, Oliver Müller, Jun Yu, Joseph J.Y. Sung and Peter Malfertheiner

in Carcinogenesis

Volume 23, issue 1, pages 87-91
Published in print January 2002 | ISSN: 0143-3334
Published online January 2002 | e-ISSN: 1460-2180 | DOI:
Increased β-catenin mRNA levels and mutational alterations of the APC and β-catenin gene are present in intestinal-type gastric cancer

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β-Catenin is critical for intercellular adhesion and also plays a role as a transcription activating protein in the Wnt signalling pathway. Increased protein levels and mutation of the β-catenin gene have been demonstrated in various cancers; however, the role of β-catenin in gastric cancer remains largely unknown. Using gastric cancer tissues and normal adjacent gastric mucosa obtained from 20 patients with gastric cancer (eight diffuse-type, 12 intestinal-type) undergoing gastric resection or endoscopy, we assessed the expression of β-catenin by immunohistochemistry and quantitative PCR analysis. Furthermore, the tumour suppressor gene APC, which down-regulates the β-catenin levels was analysed for mutations. Overall mRNA levels of β-catenin were significantly increased in the tumour samples compared with the matched normal gastric mucosa (P < 0.05). Increased β-catenin mRNA levels were significantly more frequent in intestinal-type gastric cancers as compared to diffuse-type gastric cancers (P < 0.01). Six out of 20 tumours exhibited >6-fold increased β-catenin mRNA levels as compared with normal mucosa. APC gene mutations were found in four cases. A β-catenin gene mutation was identified only in one intestinal-type gastric cancer exhibiting a massive overexpression of β-catenin mRNA in the tumour. In intestinal-type gastric cancers β-catenin mRNA levels are greatly enhanced. APC and β-catenin gene mutations are also present primarily in intestinal-type gastric cancers. These findings support the hypothesis that in intestinal-type gastric cancers the accumulation of β-catenin protein may result from impaired degradation of the β-catenin protein due to alterations of the β-catenin and APC genes, as well as from enhanced β-catenin transcription which is present in the great majority of intestinal-type gastric cancers.

Keywords: cDNA, complementary DNA; MDE, mutation detection enhancement; PCR, polymerase chain reaction; RT, reverse transcription; SSCP, single-strand conformation polymorphism

Journal Article.  4425 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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