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Department of Pathology and Cancer Research Institute, Catholic University Medical College, Seoul 137-701 [S. M. D., K. M. K., Su Y. K., M. S. S., E. Y. N., S. H. L., W. S. P., N. J. Y., J. W. K., Se Y. K., S. H. K., C. S. K., J. Y. L.]; Department of Pathology, Seoul National University College of Medicine, and Cancer Research Center, Seoul 110-799 [J. J. J.]; Korea Food and Drug Administration, Seoul 122-020 [C. Y. Y.]; and Genetic Laboratory of Premedical Course, Kon-Kuk University College of Medicine, Chung-Ju 380-060 [Y. M. Y.], Korea
We analyzed somatic mutation and loss of heterozygosity (LOH) in the serine/threonine kinase 11 (STK11)/Peutz-Jeghers syndrome gene in 49 colorectal tumors in three different stages of a dysplasia-carcinoma sequence. We detected LOH in 10 of 19 (52.6%) informative colorectal cancers at loci D19S886 and/or D19S883, but no LOH was observed in 25 informative adenomas. We detected a total of 9 somatic mutations [7 of 13 (53.8%) left-sided colon cancers and 2 of 7 (28.6%) left-sided adenomas with high-grade dysplasia], but no mutations were detected in right-sided colon tumors. Of the nine mutations, one was a frameshift mutation (the same mutation detected in Peutz-Jeghers syndrome family previously), and the other eight were missense mutations. This results indicate that STK11 is a tumor suppressor gene and that genetic changes of STK11 play an important role in left-sided colon cancer carcinogenesis.
1 This work was supported by funding from the "Good Health R&D Project" of the Ministry of Health Welfare of Korea (Grant HMP-98-M-2-0018).
2 The first two authors contributed equally to this study.
3 To whom requests for reprints should be addressed, at Dept. of Pathology, Catholic University Medical College, Seoul 137-701, Korea.
Received 4/23/98. Accepted 7/17/98.
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