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Analysis of Loss of Heterozygosity on Chromosome 11 and Infrequent Inactivation of the MEN1 Gene in Sporadic Pituitary Adenomas¹

Otsuka Department of Clinical and Molecular Nutrition (C.T., M.M., T.Y., K.Y., M.I.), First Department of Internal Medicine (T.K.), and First Department of Pathology (P.Y., T.S.), University of Tokushima School of Medicine, 3–18-15 Kuramoto-cho, Tokushima 770-8503; and the Department of Neurosurgery, Toranomon Hospital (S.Y.), 2–2-2 Toranomon, Minato-ku, Tokyo 105-0001, Japan

Address all correspondence and requests for reprints to: Katsuhiko Yoshimoto, M.D., Ph.D., Otsuka Department of Clinical and Molecular Nutrition, University of Tokushima School of Medicine, 3–18-15 Kuramoto-cho, Tokushima 770-8503, Japan.

To investigate the role of tumor suppressor genes in sporadic pituitary adenomas, we first analyzed loss of heterozygosity on 11q13 with microsatellite analysis in 31 tumors. Loss of heterozygosity on 11q13 was detected in 1 mixed GH/PRL adenoma, and the somatic 22-bp deletion of the multiple endocrine neoplasia type 1 (MEN1) gene encoding menin was detected in this tumor. Trisomy 11 suggested by the decreased mean allelic ratios of 66% or 65% for 16 or 13 microsatellite markers, respectively, in 2 of 31 pituitary adenomas was confirmed by interphase fluorescence in situ hybridization. Screening for mutations of the MEN1 gene did not find mutations with PCR-single strand conformation polymorphism analysis in other pituitary adenomas retaining heterozygosity on 11q13.

Based on these, it is concluded that inactivation of the MEN1 gene comprises a rare etiology for tumorigenesis of the pituitary gland, and that trisomy 11 or another gene(s) may contribute to the pathogenesis of sporadic pituitary adenomas.

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