Abstract
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.
Footnotes
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↵1 This work was funded by Grant 2541 from the Tobacco Research Council.
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↵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 March 1, 1990.
- Accepted July 16, 1990.
- ©1990 American Association for Cancer Research.
Volume 50, Issue 20
