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Online edition:ISSN 2434-3404

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Cytogenetic analysis of secondary hyperparathyroidism *

Secondary hyperparathyroidism is a common endocrine disorder in uremic patients, and has been considered as an adaptic physiologic response to this state. However, a recent study using X-chromosome inactivation analysis to evaluate clonality showed that 64% of uremic patients had at least one monoclonal parathyroid tumor. The molecular basis of parathyroid tumorigenesis has been shown to involve overexpression of the cyclin D1 oncogene and loss of the MEN1 tumor suppressor gene, but much still remains unclear. To find the loci involved in parathyroid tumorigenesis in secondary hyperparathyroidsm (2 HPT), a chromosome study and an LOH (Loss of heterozygosity) study were performed. For the chromosome study, 15 fresh parathyroid tissue samples obtained from 15 hemodialysis patients with 2 HPT who had undergone parathyroidectomy were analyzed. G-band analysis was performed. For the LOH study, high molecular weight DNA extracted from 42 parathyroid tumors and the peripheral leukocytes of the patients with 2 HPT were analyzed. The microsatellite markers located around the loci of multiple endocrine neoplasia type I (11 q 13), hyperparathyroidism jaw tumor syndrome (1 q 21-32) and the calcium sensing receptor (2 q 21―q 22), were analyzed. Chromosome markers that showed abnormality in the G-band analysis were also analyzed. Among the 15 tissue samples, the G-band analysis could be completed in thirteen. Seven samples had an abnormality and the other six samples were normal. An increase in chromosome 7 was found in 38% (5/13) and loss of chromosome 22 was noted in 23% (3/13). In the LOH study, 19% (8/42) of the samples showed LOH on the chromosome 22 markers and 7% (3/42) on the chromosome 11 markers. This study suggests that several chromosomal loci are important for tumor formation. Specifically chromosomes 7 and 22 might play an important role in the tumorigenesis of 2 HPT. (Acceptcd on Octobor 17, 2001) Kawasaki Igakkaishi 27(4 ) : 315 - 322, 2001

Author
Tokura T.
Volume
27
Issue
4
Pages
315-322
DOI
10.11482/KMJ27(4)315-322.2001.pdf

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