Accumulation of nonphosphorylated β-catenin and c-myc in primary and uremic secondary hyperparathyroid tumors

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Björklund, PeymanUppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery (författare)

Accumulation of nonphosphorylated β-catenin and c-myc in primary and uremic secondary hyperparathyroid tumors

Artikel/kapitelEngelska2007

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The Endocrine Society,2007
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LIBRIS-ID:oai:DiVA.org:uu-96470
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-96470URI
https://doi.org/10.1210/jc.2006-1197DOI

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Språk:engelska
Sammanfattning på:engelska

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Ämneskategori:ref swepub-contenttype
Ämneskategori:art swepub-publicationtype

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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.

Ämnesord och genrebeteckningar

Kidney disease
Urinary system disease
Endocrinology
Secondary
Primary
Tumor
Protooncogene
myc Gene
Renal failure
C-Onc gene
Accumulation
β Catenin
MEDICINE
MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

Åkerström, GöranUppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery(Swepub:uu)goranas (författare)
Westin, GunnarUppsala universitet,Institutionen för kirurgiska vetenskaper,Endokrinkirurgi, Endocrine Surgery(Swepub:uu)gunnwest (författare)
Uppsala universitetInstitutionen för kirurgiska vetenskaper (creator_code:org_t)

Sammanhörande titlar

Ingår i:Journal of Clinical Endocrinology and Metabolism: The Endocrine Society92:1, s. 338-3440021-972X1945-7197

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Journal of Clinical Endocrinology and Metabolism (Sök värdpublikationen i LIBRIS)

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Av författaren/redakt...: Björklund, Peyma ...; Åkerström, Göran; Westin, Gunnar

Artiklar i publikationen: Journal of Clini ...

Av lärosätet: Uppsala universitet

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