| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Misa Department of Pathology, Wakayama Medical University, instructor, 医学部, 助手 (70285386)
NAKAMAURA Yasushi Department of Pathology, Wakayama Medical University, instructor, 医学部, 助手 (60275352)
UTUNOMIYA Hirotosi Department of Pathology, Wakayama Medical University, assistant professor, 医学部, 講師 (60264876)
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| Research Abstract |
It is difficult to differentiate between parathyroid neoplasia and hyperplasia. In an attempt to elucidate the clonality of uremic parathyroid hyperplasia and the molecular genetic abnormalities accounting for clonal emergence, we analyzed 20 cases of uremic parathyroid hyperplasia. Clonalities were determined using the X-chromosome-linked human androgen receptor(HUMARA) gene and the phosphoglycerate kinase(PGK) gene, and multiple endocrine neoplasia type1(MEN1) gene abnormality was analyzed by studying loss of heterozygosity(LOH) in 11q13 and somatic mutations in the MEN1 gene. As a positive control, a case of MEN1 with Zollinger-Ellison syndromes was analyzed simultaneously. Our analysis revealed that a majority(75%)of theuremic parathyroid hyperplasia tissues, in-cluding an autograft with recurrent hyperparathyroidism, was of monoclonal orig-in. Clonality did not correlate with serum carboxyl-terminal parathyroid hormone(C-PTH) level, calcium level, hemodialytic duration, gland weight or pathological features. Neither LOH in 11q13 nor somatic mutation in the MEN1 gene was detected. For the MEN1 case, a germline mutation(W198X)was detected In exon3. We concluded that a majority of the uremic parathyroid hyperplasia cases was in fact monoclonal naeoplasia. MEN1 gene abnormality played a minor role, if any, in the clonal emergence in uremic parathyroid hyperplasia.
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