title: Mutation and expression of the beta-catenin-interacting protein ICAT in human colorectal tumors.
abstract: BACKGROUND
  Aberrant activation of Wnt signaling caused by mutations in the tumor suppressor adenomatous polyposis coli or beta-catenin is a critical event in the development of human colorectal tumors. We have recently identified the ICAT gene, which encodes a small protein that interacts with beta-catenin and represses Wnt signaling.
  
  
  METHODS
  We examined the prevalence of mutations in the entire ICAT coding sequence and intronic splice donor and acceptor regions of ICAT by PCR-SSCP and also the expression of the ICAT gene by RT-PCR.
  
  
  RESULTS
  The ICAT gene was mapped to chromosome 1p36.1-p36.2, which is implicated in the pathogenesis of various types of cancers. However, no mutations in ICAT were detected among 128 colorectal tumors. Instead, ICAT was found to be overexpressed in almost half of colorectal carcinomas. Cases exhibiting ICAT overexpression showed a significantly higher incidence of well-differentiated adenocarcinoma and positive lymphatic permeation.
  
  
  CONCLUSIONS
  Our results suggest that ICAT is not the putative tumor suppressor on 1p36.1-p36.2, although aberrant overexpression of ICAT may play a role in the pathogenesis of colorectal carcinomas.
authors.affiliation: Second Department of Surgery, Gunma University School of Medicine, Maebashi, Laboratory of Molecular and Genetic Information, Institution of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Koyama
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Tago
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nakamura
authors.forename: Susumu
authors.initials: S
authors.lastname: Ohwada
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Morishita
authors.forename: Jun
authors.initials: J
authors.lastname: Yokota
authors.forename: Tetsu
authors.initials: T
authors.lastname: Akiyama
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D011125:Adenomatous Polyposis Coli / Q000235:genetics; D000368:Aged; D018797:Cell Cycle Proteins; D003110:Colonic Neoplasms / Q000235:genetics* / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000096:biosynthesis* / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D017491:Genes, APC; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins / Q000096:biosynthesis / Q000235:genetics*; D009154:Mutation; D016133:Polymerase Chain Reaction; D018807:Polymorphism, Single-Stranded Conformational; D012004:Rectal Neoplasms / Q000235:genetics* / Q000378:metabolism; D012097:Repressor Proteins; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015534:Trans-Activators / Q000096:biosynthesis*; D051176:beta Catenin
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C495270:CTNNB1 protein, human; C411982:CTNNBIP1 protein, human; D018797:Cell Cycle Proteins; D003598:Cytoskeletal Proteins; D047908:Intracellular Signaling Peptides and Proteins; D009124:Muscle Proteins; D012097:Repressor Proteins; D015534:Trans-Activators; D051176:beta Catenin