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Infrequent Mutations of p27^Kip1 Gene and Trisomy 12 in a Subset of Human Pituitary Adenomas¹

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

Address all correspondence and requests for reprints to: Mitsuo Itakura, M.D., Ph.D., Otsuka Department of Clinical and Molecular Nutrition, School of Medicine, The University of Tokushima, 3–18-15, Kuramoto-cho, Tokushima-city, 770 Japan. E-mail: itakura{at}nutr.med.tokushima-u.ac.jp

To study the etiologic roles of genes on chromosome 12 for the pituitary tumorigenesis of adenomas, mutations of the p27^Kip1 gene and allelic ratios of 18 microsatellite markers on the entire chromosome 12 were studied in 33 pituitary adenomas. The p27^Kip1 gene on chromosome 12p12-p13 encoding an inhibitor of complexes between cyclins and cyclin-dependent kinases is supposed to function as the tumor suppressor gene. Among 31 sporadic and 2 familial pituitary adenomas, PCR-single strand conformation polymorphism analysis detected three polymorphic changes but no tumor-specific mutations of the p27^Kip1 gene. Genotyping of 18 microsatellite markers on the entire chromosome 12 detected the uniformly decreased allelic ratios ranging from 54–66% in 8 of 33 pituitary adenomas (24%), although no loss of heterozygosity was detected. Fluorescence in situ hybridization confirmed trisomy 12 in all 5 available samples out of these 8 samples. Based on these, we conclude that not mutations of the p27^Kip1 gene, but trisomy 12 may be etiologically important in a subgroup of pituitary adenomas.

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