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Somatic mutations of the β-TrCP gene in gastric cancer

Authors


  • Received 20 July 2006.

    Accepted 25 September 2006.

  • Chang Jae Kim and Jae Hwi Song contributed equally to this work.

Won Sang Park, Department of Pathology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Seocho-gu, Seoul 137-701, Korea. e-mail: wonsang@catholic.ac.kr

Abstract

Beta-TrCP is a component of the ubiquitin ligase complex targeting β-catenin for proteasomal degradation, and is a negative regulator of Wnt/β-catenin signaling. To determine whether genetic alterations of the β-TrCP gene are involved in the development or progression of gastric cancer, we analyzed its somatic mutations in 95 gastric cancers by single-strand conformational polymorphism and sequencing. We found five missense mutations (5.3%): A99V, H342Y, H425Y, C206Y, and G260E. Tissue carrying mutations showed moderate to strong cytoplasmic and/or nuclear staining of β-catenin by immunohistochemistry. Thus, somatic mutations of the β-TrCP gene may contribute to the development of gastric cancer through β-catenin stabilization.

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