Skip Navigation

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Inagaki, C.
Right arrow Articles by Gogusev, J.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Inagaki, C.
Right arrow Articles by Gogusev, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrology Dialysis Transplantation, Vol 13, Issue 2 348-355, Copyright © 1998 by Oxford University Press

ORIGINAL ARTICLES

Structural analysis of gene marker loci on chromosomes 10 and 11 in primary and secondary uraemic hyperparathyroidism

C Inagaki, M Dousseau, N Pacher, E Sarfati, T Drueke and J Gogusev
INSERM Unite 90, Hopital Necker, 161 rue de Sevres, F-75743 Paris, France; Service de Chirurgie Generale, Hopital Saint Louis, Paris, France; Corresponding author

Background. The genetic molecular anomalies in patients with primary (I°) and secondary (II°) hyperparathyroidism (HPTH) are still largely unknown. In particular, the changes underlying monoclonal growth in the parathyroids of patients with II° HPTH are not well understood. Methods. We screened genomic DNA from a total of 30 patients with I° HPTH and 29 patients with II° uraemic HPTH for possible rearrangement or allelic losses of several gene markers located on chromosome 11p near the PTH gene, namely Ha-ras, IGF-2, WT1, and the PTH gene itself. In addition, two other gene markers, PRAD1 (localized on 11q13) and RET localized on 10q11) were examined for possible structural alterations. Moreover, we used fluorescence in situ hybridization (FISH) which is another technique to detect numerical alterations of chromosome 11. Results. The results show that one of 13 patients with I° HPTH (8%) exhibited a rearrangement for the PRAD-1 gene. Loss of heterozygosity of Ha-ras locus was observed in one of 11 uraemic patients with II° HPTH (9%). Three of 10 patients with I° HPTH (30%) and one of 7 patients with II° HPTH (14%) showed an allelic loss of the WT1 gene. No evidence of rearrangement of allelic loss was detected for the IGF-2, PTH or RET genes respectively. Using FISH method, three normal parathyroid glands, six I° HPTH adenomas and eight II° HPTH hyperplastic glands from uraemic patients were studied with centromeric probe for chromosome 11. Monosomy 11 was observed in one case of I° HPTH and in one other case of II° HPTH. Conclusion. Evidence of loss of heterozygosity for several genes located on human chromosome 11p has been found in a series of parathyroid glands from several patients with I° and II° uraemic HPTH, corresponding to monosomy of chromosome 11 11 in some cases. Keywords: hyperparathyroidism; primary; secondary; chronic renal failure; haemodialysis; PRAD1; Ha-ras; WT1; RET; allelic loss; rearrangement; Southern blot; fluorescence in situ hybridization (FISH)
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.