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[Cancer Research 55, 5545-5547, December 1, 1995]
© 1995 American Association for Cancer Research
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A Transforming Growth Factor ß Receptor Type II Gene Mutation Common in Colon and Gastric but Rare in Endometrial Cancers with Microsatellite Instability1

Lois L. Myeroff, Ramon Parsons, Seong-Jin Kim, Lora Hedrick, Kathleen R. Cho, Kim Orth, Michael Mathis, Kenneth W. Kinzler, James Lutterbaugh, Keunchil Park, Yung-Jue Bang, Hwa Young Lee, Jae-Gahb Park, Henry T. Lynch, Anita B. Roberts, Bert Vogelstein and Sanford D. Markowitz2

Department of Medicine, Case Western Reserve University and Ireland Cancer Center, University Hospitals of Cleveland, Cleveland, Ohio 44106 [L. L. M., J. L., S. D. M.]; Department of Pathology [L. H., K. R. C.] and Johns Hopkins University Oncology Center [R. P., L. H., K. R. C., K. W. K., B. V.] Johns Hopkins University, Baltimore, Maryland 21231; Howard Hughes Medical Institute, Chevy Chase, Maryland 20815 [B. V.]; Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892 [S-J. K., K. P., H. Y. L., A. B. R.]; Division of Molecular Medicine and Genetics, University of Michigan, Ann Arbor, Michigan 48109 [K. O.]; Simmons Cancer Center, University of Texas Southwestern Medical School, Dallas, Texas 75235 [M. M.]; Cancer Research Center, Seoul National University College of Medicine, Seoul, Korea [Y-J. B., J-G. P.]; and Department of Preventive Medicine and Public Health, Creighton University School of Medicine, Omaha, Nebraska 68178 [H. T. L.]

We have recently demonstrated that mutation of the transforming growth factor-ß (TGF-ß) receptor type II (RII) gene is characteristic of colon cancers exhibiting microsatellite instability or replication errors (RER+). Moreover, we have shown that RII mutations in these RER+ colon cancers are characteristically frameshift mutations within a 10-bp polyadenine repeat present in the RII-coding region. We now show that RII gene mutations in this polyadenine repeat are also commonly present in RER+ gastric cancers (71%). In contrast, we find these same RII gene mutations are distinctly uncommon in RER+ endometrial cancers (17%, P < 0.02). These results suggest that RII gene mutations confer a growth advantage and are selected for in RER+ cancers of both the upper and lower gastrointestinal tract. The genesis of RER+ endometrial tumors must, however, be by a different route.

1 Supported by NIH Grants CA57208 and P01 CA51183 (S. D. M.); P30 CA4370301 to the Case Western Reserve University Cancer Center; CA09320 (R. P.), CA68769 (K. O.), CA66720 (L. H.), CA62924 (K. W. K.), and CA35494 (B. V.); American Cancer Society Grants FRA-451 (S. M.), RD-381 (H. L.), and EDT-84 (H. L.); Council for Tobacco Research Grant 1297ER1 (H. L.); Korea Science and Engineering Foundation Grant KOSEF-SRC-56-CRC-94K3-0401-01-03-3 (Y-J. B., J-G. P.); and by grants from the Ohio Cancer Research Associates (S. M.) and the Clayton Fund (B. V.). B. V. is an investigator of the Howard Hughes Medical Institute.

2 To whom request for reprints should be addressed, at Ireland Cancer Center, University Circle Research Center 2, Room 200, 11001 Cedar Road, Cleveland, OH 44106.

Received 10/ 6/95. Accepted 10/25/95.




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