{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:18:07Z","timestamp":1784557087202,"version":"3.55.0"},"reference-count":132,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:p>\n                    Five syndromes share predominantly hyperplastic glands with a primary excess of hormones: neonatal severe primary hyperparathyroidism, from homozygous mutated\n                    <jats:italic>CASR<\/jats:italic>\n                    , begins severely\n                    <jats:italic>in utero<\/jats:italic>\n                    ; congenital non-autoimmune thyrotoxicosis, from mutated\n                    <jats:italic>TSHR<\/jats:italic>\n                    , varies from severe with fetal onset to mild with adult onset; familial male-limited precocious puberty, from mutated\n                    <jats:italic>LHR<\/jats:italic>\n                    , expresses testosterone oversecretion in young boys; hereditary ovarian hyperstimulation syndrome, from mutated\n                    <jats:italic>FSHR<\/jats:italic>\n                    , expresses symptomatic systemic vascular permeabilities during pregnancy; and familial hyperaldosteronism type IIIA, from mutated\n                    <jats:italic>KCNJ5<\/jats:italic>\n                    , presents in young children with hypertension and hypokalemia. The grouping of these five syndromes highlights predominant hyperplasia as a stable tissue endpoint and as their tissue stage for all of the hormone excess. Comparisons were made among this and two other groups of syndromes, forming a continuum of gland staging: predominant oversecretions express little or no hyperplasia; predominant hyperplasias express little or no neoplasia; and predominant neoplasias express nodules, adenomas, or cancers. Hyperplasias may progress (5 of 5) to neoplastic stages while predominant oversecretions rarely do (1 of 6; frequencies differ\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.02). Hyperplasias do not show tumor multiplicity (0 of 5) unlike neoplasias that do (13 of 19;\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.02). Hyperplasias express mutation of a plasma membrane-bound sensor (5 of 5), while neoplasias rarely do (3 of 14;\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.002). In conclusion, the multiple distinguishing themes within the hyperplasias establish a robust pathophysiology. It has the shared and novel feature of mutant sensors in the plasma membrane, suggesting that these are major contributors to hyperplasia.\n                  <\/jats:p>","DOI":"10.1530\/erc-15-0171","type":"journal-article","created":{"date-parts":[[2015,9,25]],"date-time":"2015-09-25T20:28:25Z","timestamp":1443212905000},"page":"R1-R14","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":13,"title":["Hyperplasia in glands with hormone excess"],"prefix":"10.1530","volume":"23","author":[{"given":"Stephen J","family":"Marx","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"2015112318390657000_23.1.R1.1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2008-2083"},{"key":"2015112318390657000_23.1.R1.2","doi-asserted-by":"crossref","unstructured":"Arnold A 2011 Pathogenesis of endocrine tumors. 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