Cancer Res  1999 Sep 1;59(17):4257-60 

Frequent somatic mutations of the beta-catenin gene in intestinal-type gastric
cancer.

Park WS, Oh RR, Park JY, Lee SH, Shin MS, Kim YS, Kim SY, Lee HK, Kim PJ, Oh ST,
Yoo NJ, Lee JY.

Department of Pathology and Cancer Research Institute, Catholic University
Medical College, Seoul, Korea.

The increased level of cytoplasmic beta-catenin through the mutations to either
beta-catenin or adenomatous polyposis coli (APC) has been proposed as an
important oncogenic step in various tumors. Gastric cancer showed frequent
genetic alterations of the APC gene, and the risk for gastric cancer in familial
adenomatosus polyposis patients is 10 times higher than that in the general
population. These findings raise the possibility that mutations of beta-catenin
may also be associated with the development of gastric cancer. We detected seven
somatic mutations in a portion of exon 3 encoding for the glycogen synthase
kinase 3beta phosphorylation consensus region of the beta-catenin gene in 43
gastric cancers. All of these mutations were missense mutations, of which five
are in the highly conserved aspartic acid 32 and two are in serine 29; all of
these seven mutations were detected exclusively in intestinal-type gastric
cancers (7 of 26; 26.9%), but not in the diffuse-type (0 of 17). We concluded
that disruption of the APC/beta-catenin/T cell factor-lymphoid enhancer binding
factor pathway might play an important role especially in the development of
intestinal-type gastric cancer.

PMID: 10485468 [PubMed - indexed for MEDLINE]