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[Cancer Research 59, 4257-4260, September 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4257-4260, September 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Frequent Somatic Mutations of the ß-Catenin Gene in Intestinal-Type Gastric Cancer1

Won Sang Park, Ro Ra Oh, Jik Young Park, Sug Hyung Lee, Min Sun Shin, Young Sil Kim, Su Young Kim, Hyun Kyung Lee, Pum Joon Kim, Seong Taek Oh, Nam Jin Yoo and Jung Young Lee2

Department of Pathology and Cancer Research Institute [W. S. P., R. R. O., J. Y. P., S. H. L., M. S. S., Y. S. K., S. Y. K., H. K. L., P. J. K., N. J. Y., J. Y. L.] and Department of Surgery [S. T. O.], Catholic University Medical College, Seoul 137-701 Korea

The increased level of cytoplasmic ß-catenin through the mutations to either ß-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 ß-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 3ß phosphorylation consensus region of the ß-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/ß-catenin/T cell factor-lymphoid enhancer binding factor pathway might play an important role especially in the development of intestinal-type gastric cancer.




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