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Loss of Heterozygosity of Markers on Chromosome 11 in Tumors from Patients with Multiple Endocrine Neoplasia Syndrome Type 1¹

Department of Surgery, St. Louis University School of Medicine [D. M. R.], and Departments of Surgery [S. W. A., S. A. W.] and Genetics [D. S. G.], Washington School of Medicine, St. Louis, Missouri 63110

Multiple endocrine neoplasia type 1 is an autosomal dominant condition characterized by the development of parathyroid hyperplasia, pituitary adenomas, and pancreatic islet cell tumors. Recently the gene for multiple endocrine neoplasia type 1 was mapped to the long arm of chromosome 11 between the loci PGA and INT2. We tested the hypothesis that tumor development is the result of a somatic deletion that unmasks a constitutional mutation. By investigating DNA isolated from tumors and somatic tissues in 12 patients from 4 different families with multiple endocrine neoplasia type 1, we found loss of heterozygous markers mapped to 11q13 in 9 (82%) of 11 informative tumors. In contrast, we were unable to identify allelic loss from other chromosomes using a variety of informative probes. This high incidence of chromosomal deletion of 11q13 suggest that this region is important in the oncogenesis of this disorder.

¹ This work was funded by Grant 2541 from the Tobacco Research Council.

² To whom requests for reprints should be addressed, at Department of Genetics, Washington University School of Medicine, 660 South Euclid Boulevard, St. Louis, MO 63110.

Received 3/ 1/90. Accepted 7/16/90.

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