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Somatic mutations of the β‐TrCP gene in gastric cancer
Author(s) -
KIM CHANG JAE,
SONG JAE HWI,
CHO YONG GU,
KIM YOUNG SILL,
KIM SU YOUNG,
NAM SUK WOO,
YOO NAM JIN,
LEE JUNG YOUNG,
PARK WON SANG
Publication year - 2007
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2007.apm_562.x
Subject(s) - somatic cell , missense mutation , biology , gene , cancer research , wnt signaling pathway , mutation , cancer , ubiquitin ligase , gene mutation , microbiology and biotechnology , genetics , ubiquitin
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.