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Departments of Molecular Pathology [H. Ou., H. O. S., A. H.], Pathology [H. Oh.], and Surgery [K. M., T. A., K. S.], Tohoku University School of Medicine, Sendai 980-77; Hitachi Electronics Engineering Co., Ltd., 3-16-3 Higashi, Shibuya-ku, Tokyo 150 [H. H.]; Department of Pathology, Cancer Institute, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170 [Y. K.], Japan; and Gastrointestinal Division, Department of Medicine, University of Maryland School of Medicine and Baltimore Veterans Affairs Medical Center, Baltimore, Maryland 21201 [R. F. S., S. J. M.]
Disruption of the DNA mismatch repair system, characterized by microsatellite instability (MI), plays an important role in the course of human carcinogenesis. Repetitive sequences constitute targets for mutation in MI+ cells, and frequent mutations have indeed been reported in such regions within the transforming growth factor ß receptor II (RII) gene in genetically unstable colorectal and gastric cancers. However, other genes that are targets for mutations in MI+ cells during the course of carcinogenesis have proven elusive. Because the insulin-like growth factor II receptor (IGFIIR) gene contains several repetitive sequences within its coding region, we examined mutations of this gene in MI+ cancers occurring at various primary sites. We found frameshift mutations in the poly(G)8 tract of IGFIIR in eight tumors, all of which were MI+: 4 of 26 (15%) MI+ endometrial cancers, 3 of 12 (25%) MI+ gastric cancers, and 1 of 18 (6%) MI+ colorectal cancers. In contrast, no mutation was found in 51 pancreatic cancers, 7 of which (14%) were MI+. These results implicate abnormal IGFIIR-mediated growth control in carcinogenesis involving the endometrium, stomach, and colorectum but not the pancreas.
1 This work was supported in part by the Ministry of Education, Science, Sports and Culture of Japan, the Vehicle Racing Commemorative Foundation, the Uehara Memorial Foundation, the Chiyoda Mutual Life Foundation, the Yasuda Medical Research Foundation, the Takeda Science Foundation, and the Ichiro Kanehara Foundation.
2 To whom requests for reprints should be addressed. Phone: 81-22-717-8042; Fax: 81-22-717-8047; E-mail: horii@mail.cc.tohoku.ac.jp.
Received 2/ 3/97. Accepted 4/ 1/97.
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