Cancer Lett  2000 Oct 16;159(1):73-8 

Activation of the beta-catenin gene by interstitial deletions involving exon 3
as an early event in colorectal tumorigenesis.

Murata M, Iwao K, Miyoshi Y, Nagasawa Y, Yabu M, Himeno S, Imanishi K, Ohsawa M,
Wada H, Tominaga S, Shimano T, Kobayashi T, Nakamura Y.

Department of Surgery, Ikeda Municipal Hospital, 3-1-18 Jyonan, Ikeda-shi,
563-8510, Osaka, Japan. muratamasaru@mth.biglobe.ne.jp

beta-Catenin has been identified as an oncogene in several tumors including
colorectal cancers. beta-Catenin gene is activated by interstitial deletions
involving exon 3 in colorectal carcinomas of Japanese population, in contrast to
amino acid substitutions detected among Caucasian population. The aim of this
study was to examine the type and frequency of beta-catenin gene mutation during
early stages of colorectal tumorigenesis. We screened 100 colorectal adenomas
for somatic mutations in the beta-catenin gene by single-strand conformation
polymorphism method, as well as polymerase chain reaction amplification. In
cases with mutations, sequencing analyses and immunohistochemical staining were
also performed. Somatic interstitial deletions of 272-413 bp, each of which
included all parts of exon 3, were detected in three tumors. However, no adenoma
carried missense mutations. We confirmed accumulation of aberrant beta-catenin
protein in cytoplasm and nuclei of adenoma cells by immunohistochemical
analysis. Our results suggested that activation of the beta-catenin gene by
interstitial deletions involving exon 3 might be less frequent compared with
frequent alterations of adenomatous polyposis coli (APC) gene, but could be an
early event in colorectal tumorigenesis equivalent to APC gene alterations in
the Japanese population.

PMID: 10974408 [PubMed - indexed for MEDLINE]