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Molecular Pathophysiology [E. F., A. M. S.] and Metabolic Diseases [L. D. M., G. D. A., S. J. M.] Branches, National Institute of Diabetes, Digestive, and Kidney Diseases; the Clinical Neurogenetics Branch [P. V. G.], National Institute of Mental Health; and Surgery Branch [J. A. N.], National Cancer Institute, Bethesda, Maryland 20892, and the Department of Human Genetics [A. E. B.], Yale University School of Medicine, New Haven, Connecticut 06510
1 To whom requests for reprints should be addressed, at Department of Clinical Genetics, Karolinska Hospital, P.O. Box 60500, S-104 01, Stockholm, Sweden.
Parathyroid tumors may occur in a sporadic fashion or, more rarely, as part of a familial syndrome (such as familial multiple endocrine neoplasia type I). The MENI gene has been mapped by linkage analysis to chromosome 11 at band q11-q13, and presumably acts as a tumor suppressor gene. In the present study, which is an extension of our previous studies, we examined 41 parathyroid tumors from patients with familial multiple endocrine neoplasia type I and 61 sporadic parathyroid tumors with markers on chromosome 11, to assess the extent of allelic loss in those tumors. Twenty-four of the MENI-associated tumors (58%) and 16 of the sporadic parathyroid tumors (26%) displayed allelic loss from chromosome 11. The region of overlap of the allelic losses in the MENI-associated tumors enables us to place the MENI gene between PGA centromerically and INT2 telomerically, a region spanning about 7.5 cM. Taken together with locus ordering by linkage analysis, this clearly localizes the MENI gene telomeric to the PGA locus. Our inability to detect allelic loss on chromosome 11 in some parathyroid tumors suggests the existence of other genes involved in the development and/or progression of this subgroup of presumably monoclonal tumors; or that localized events involving the 11q tumor suppressor gene have occurred in some parathyroid tumors whose detection is beyond the sensitivity of our analysis; or that at least some of the specimens analyzed were in fact primarily hyperplastic parathyroid tissue.
2 Supported by CNPq and FAPEMIG, Brazil.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 8/14/92. Accepted 9/30/92.
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