{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T16:58:58Z","timestamp":1791305938077,"version":"4.3.1"},"reference-count":35,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:p>\n                    Primary hyperparathyroidism (pHPT) resulting from parathyroid tumors is a common endocrine disorder with incompletely understood etiology. In renal failure, secondary hyperparathyroidism (sHPT) occurs with multiple tumor development as a result of calcium and vitamin D regulatory disturbance. The aim of this study was to investigate a potential role of the histone 3 lysine 27 methyltransferase EZH2 in parathyroid tumorigenesis. Parathyroid tumors from patients with pHPT included adenomas and carcinomas. Hyperplastic parathyroid glands from patients with HPT secondary to uremia and normal parathyroid tissue specimens were included in this study. Quantitative RT-PCR, western blotting, bisulfite pyrosequencing, colony formation assay, and RNA interference were used.\n                    <jats:italic>EZH2<\/jats:italic>\n                    was overexpressed in a subset of the benign and in all malignant parathyroid tumors as determined by quantitative RT-PCR and western blotting analyses. Overexpression was explained by\n                    <jats:italic>EZH2<\/jats:italic>\n                    gene amplification in a large fraction of tumors.\n                    <jats:italic>EZH2<\/jats:italic>\n                    depletion by RNA interference inhibited sHPT-1 parathyroid cell line proliferation as determined by tritium\u2013thymidine incorporation and colony formation assays.\n                    <jats:italic>EZH2<\/jats:italic>\n                    depletion also interfered with the Wnt\/\u03b2-catenin signaling pathway by increased expression of growth-suppressive\n                    <jats:italic>AXIN2<\/jats:italic>\n                    , a negative regulator of \u03b2-catenin stability. Indeed,\n                    <jats:italic>EZH2<\/jats:italic>\n                    contributed to the total level of aberrantly accumulated transcriptionally active (nonphosphoylated) \u03b2-catenin in the parathyroid tumor cells. To our knowledge\n                    <jats:italic>EZH2<\/jats:italic>\n                    gene amplification presents the first genetic aberration common to parathyroid adenomas, secondary hyperplastic parathyroid glands, and parathyroid carcinomas. This supports the possibility of a common pathway in parathyroid tumor development.\n                  <\/jats:p>","DOI":"10.1530\/erc-13-0497","type":"journal-article","created":{"date-parts":[[2013,11,29]],"date-time":"2013-11-29T21:42:48Z","timestamp":1385761368000},"page":"231-239","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":46,"title":["The histone methyltransferase EZH2, an oncogene common to benign and malignant parathyroid tumors"],"prefix":"10.1530","volume":"21","author":[{"given":"Jessica","family":"Svedlund","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elham","family":"Barazeghi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"St\u00e5lberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per","family":"Hellman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00f6ran","family":"\u00c5kerstr\u00f6m","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peyman","family":"Bj\u00f6rklund","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gunnar","family":"Westin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"issue":"1","key":"1_17963262","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1097\/00001622-200401000-00002","volume":"16","author":"Akerstr\u00a0\u00a0m","year":"2004","journal-title":"Current opinion in oncology","ISSN":"https:\/\/id.crossref.org\/issn\/1040-8746","issn-type":"print"},{"issue":"11","key":"2_34619295","doi-asserted-by":"publisher","first-page":"2224","DOI":"10.1007\/s00268-009-0022-6","volume":"33","author":"Westin","year":"2009","journal-title":"World journal of surgery","ISSN":"https:\/\/id.crossref.org\/issn\/0364-2313","issn-type":"print"},{"issue":"2","key":"3_23119739","doi-asserted-by":"publisher","first-page":"532","DOI":"10.1016\/j.bbrc.2006.11.056","volume":"352","author":"Bjorklund","year":"2007","journal-title":"Biochemical and biophysical research communications","ISSN":"https:\/\/id.crossref.org\/issn\/0006-291X","issn-type":"print"},{"issue":"1","key":"4_22814024","doi-asserted-by":"publisher","first-page":"338","DOI":"10.1210\/jc.2006-1197","volume":"92","year":"2007","journal-title":"Journal of Clinical Endocrinology &amp; 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