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Microsatellite Instability in Sporadic Parathyroid Adenoma¹

Departments of Pharmacology (M.S., W.L.B., A.F.D., L.D.) and Pathology (R.S.G.), Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil; and The Susanne Levy Gertner Oncogenetics Unit (E.F.), Institute of Genetics, Chaim Sheba Medical Center, Tel Hashomer, 52621, Israel

Address correspondence and requests for reprints to: L. De Marco, M.D., Ph.D., Av. Antonio Carlos 6627, Belo Horizonte 31270-901, Brazil. E-mail: ldemarco{at}icb.ufmg.br

Parathyroid adenomas are usually benign uniglandular tumors, and inactivation of several tumor suppressor genes, notably the MEN 1 gene, or activation of oncogenes have been implicated in the tumorigenesis. Genomic instability, indicative of the involvement of DNA mismatch repair genes, has not been previously described in parathyroid adenomas. A single large parathyroid adenoma was resected from an 8.5-yr-old Brazilian patient with no personal or family history of other endocrinopathies. Analysis of paired tumor-nontumor DNA using 23 microsatellite markers, located on chromosomes 1, 10, and 11 was carried out. Microsatellite instability was detected in nine markers (D1S191, D1S212, D1S413, D1S2848, RET, D11S901, D11S903, INSR, and INT2), whereas no allelic loss was detected with any of the analyzed markers. Immunohistochemical analysis of retinoblastoma protein expression revealed low levels of expression, but no histopathological signs of malignancy. We conclude that in this single, apparently sporadic parathyroid adenoma, DNA mismatch repair genes might be involved in parathyroid tumorigenesis.

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