Analysis of Loss of Heterozygosity on Chromosome 11 and Infrequent Inactivation of the MEN1 Gene in Sporadic Pituitary Adenomas1
| Autor: | Maki Moritani, Toshiaki Sano, Takashi Yamaoka, Katsuhiko Yoshimoto, Chisato Tanaka, Takehiko Kimura, Mitsuo Itakura, Peng Yang, Shozo Yamada |
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| Rok vydání: | 1998 |
| Předmět: |
Pituitary gland
medicine.medical_specialty endocrine system diseases medicine.diagnostic_test Adenoma Endocrinology Diabetes and Metabolism Biochemistry (medical) Clinical Biochemistry Pituitary neoplasm Biology medicine.disease Biochemistry Loss of heterozygosity Endocrinology medicine.anatomical_structure Internal medicine medicine Cancer research MEN1 Multiple endocrine neoplasia Trisomy Fluorescence in situ hybridization |
| Zdroj: | The Journal of Clinical Endocrinology & Metabolism. 83:2631-2634 |
| ISSN: | 1945-7197 0021-972X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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