Search: id:"swepub:oai:DiVA.org:uu-96470" >
Accumulation of non...
Accumulation of nonphosphorylated β-catenin and c-myc in primary and uremic secondary hyperparathyroid tumors
-
- Björklund, Peyman (author)
- Uppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery
-
- Åkerström, Göran (author)
- Uppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery
-
- Westin, Gunnar (author)
- Uppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery
-
(creator_code:org_t)
- The Endocrine Society, 2007
- 2007
- English.
-
In: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 92:1, s. 338-344
- Related links:
-
https://academic.oup...
-
show more...
-
https://urn.kb.se/re...
-
https://doi.org/10.1...
-
show less...
Abstract
Subject headings
Close
- CONTEXT: Primary hyperparathyroidism (pHPT) resulting from parathyroid tumors is a common endocrine disorder with incompletely understood etiology, affecting about 1% of the adult population, with an even higher prevalence for elderly individuals. In renal failure, secondary hyperparathyroidism (sHPT) occurs with multiple tumor development as a result of calcium and vitamin D regulatory disturbance. OBJECTIVE: Aberrant Wnt/beta-catenin signaling with accumulation of beta-catenin in the cytoplasm/nucleus is involved in the development of a variety of neoplasms. The aim of this study was to evaluate whether the Wnt/beta-catenin signaling pathway is activated in parathyroid adenomas of pHPT and in hyperplastic glands from uremic patients with sHPT. DESIGN: Immunohistochemistry, Western blotting, real-time quantitative RT-PCR, and DNA sequencing were performed. RESULTS: beta-Catenin was accumulated in all analyzed parathyroid tumors (n = 47) from patients with pHPT and from patients with HPT secondary to uremia. The accumulation included nonphosphorylated, stabilized (transcriptionally active) beta-catenin. The overexpression was not related to increased beta-catenin mRNA levels. A protein-stabilizing mutation in exon 3 of beta-catenin (S37A) was detected in three of 20 pHPT tumors (15%). No mutation was detected in secondary hyperplastic glands (n = 20), and no evidence for truncated adenomatosis polyposis coli proteins was found in adenomas and secondary hyperplastic glands. Mutations in other Wnt signaling components leading to beta-catenin accumulation, other than in beta-catenin itself, are therefore anticipated. The beta-catenin target gene c-myc was overexpressed in a substantial fraction of the parathyroid tumors. CONCLUSION: Our results strongly suggest that modifications in the Wnt/beta-catenin signaling pathway may be involved in the development of hyperparathyroidism.
Keyword
- Kidney disease
- Urinary system disease
- Endocrinology
- Secondary
- Primary
- Tumor
- Protooncogene
- myc Gene
- Renal failure
- C-Onc gene
- Accumulation
- β Catenin
- MEDICINE
- MEDICIN
Publication and Content Type
- ref (subject category)
- art (subject category)
Find in a library
To the university's database