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Genetic Abnormalities in Sporadic Parathyroid Adenomas

Molecular Pathophysiology (E.F., T.T., A.M.S.) and Metabolic Diseases (S.J.M., G.D.A.) Branches, National Institute of Diabetes, Digestive and Kidney Diseases, and the Division of Cancer Treatment, Surgery Branch, National Cancer Institute (J.A.N.), National Institutes of Health Bethesda, Maryland 20892
Department of Human Genetics, Yale University School of Medicine (A.E.B.) New Haven, Connecticutt 06510
Endocrine Unit, Massachusetts General Hospital and Harvard Medical School (A.A.) Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Eitan Friedman, National Institutes of Health, Building 10, Room 8D17, Bethesda, Maryland 20892.

We analyzed genomic DNA from 43 sporadic benign parathyroid adenomas for rearrangements of the PTH gene, and for point mutations of the H-ras (codons 12, 13, and 61), N-ras (codons 12,13, and 61), and K-ras (codons 12 and 13) genes. One of 43 parathyroid adenomas showed a chromosome 11 rearrangement involving both the PTH gene on the short arm of chromosome 11 (at band pl5) and a locus on the long arm (11ql3). This rearrangement was indistinguishable from one that was previously described in a parathyroid adenoma by Arnold et al., indicating that this may be an important contributor to tumorigenesis in a small subset of patients with parathyroid adenoma. H-ras, K-ras, and N-ras oncogene activation by point mutation at codons 12, 13, or 61, known to occur in many tumors, could not be detected in any parathyroid adenoma.

^* Dr. Arnold is the recipient of a junior faculty research award from the American Cancer Society.

Received November 30, 1989.

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