{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T23:52:04Z","timestamp":1785196324795,"version":"3.55.0"},"reference-count":461,"publisher":"The Endocrine Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,8,1]]},"abstract":"<jats:p>Hereditary origin of a tumor helps toward early discovery of its mutated gene; for example, it supports the compilation of a DNA panel from index cases to identify that gene by finding mutations in it. The gene for a hereditary tumor may contribute also to common tumors. For some syndromes, such as hereditary paraganglioma, several genes can cause a similar syndrome. For other syndromes, such as multiple endocrine neoplasia 2, one gene supports variants of a syndrome. Onset usually begins earlier and in more locations with hereditary than sporadic tumors. Mono- or oligoclonal (\u201cclonal\u201d) tumor usually implies a postnatal delay, albeit less delay than for sporadic tumor, to onset and potential for cancer. Hormone excess from a polyclonal tissue shows onset at birth and no benefit from subtotal ablation of the secreting organ. Genes can cause neoplasms through stepwise loss of function, gain of function, or combinations of these. Polyclonal hormonal excess reflects abnormal gene dosage or effect, such as activation or haploinsufficiency. Polyclonal hyperplasia can cause the main endpoint of clinical expression in some syndromes or can be a precursor to clonal progression in others. Gene discovery is usually the first step toward clarifying the molecule and pathway mutated in a syndrome. Most mutated pathways in hormone excess states are only partly understood. The bases for tissue specificity of hormone excess syndromes are usually uncertain. In a few syndromes, tissue selectivity arises from mutation in the open reading frame of a regulatory gene (CASR, TSHR) with selective expression driven by its promoter. Polyclonal excess of a hormone is usually from a defect in the sensor system for an extracellular ligand (e.g., calcium, glucose, TSH). The final connections of any of these polyclonal or clonal pathways to hormone secretion have not been identified. In many cases, monoclonal proliferation causes hormone excess, probably as a secondary consequence of accumulation of cells with coincidental hormone-secretory ability.<\/jats:p>","DOI":"10.1210\/er.2003-0037","type":"journal-article","created":{"date-parts":[[2005,7,29]],"date-time":"2005-07-29T20:52:49Z","timestamp":1122670369000},"page":"615-661","source":"Crossref","is-referenced-by-count":67,"title":["Hereditary Hormone Excess: Genes, Molecular Pathways, and Syndromes"],"prefix":"10.1210","volume":"26","author":[{"given":"Stephen J.","family":"Marx","sequence":"first","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes and Digestive"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William F.","family":"Simonds","sequence":"first","affiliation":[{"name":"Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-1802"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2005,1,4]]},"reference":[{"key":"2020071611533060900_R1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1016\/S0065-230X(08)60196-7","article-title":"Genetic epidemiology of familial aggregation of cancer.","volume":"47","author":"Schneider","year":"1986","journal-title":"Adv Cancer Res"},{"key":"2020071611533060900_R2","first-page":"81","article-title":"Sclerose tubereuse des circonvolutions cerebrales: idiotie et epilepsic hemiplegique.","volume":"1","author":"Bournville","year":"1880","journal-title":"Arch Neurol"},{"key":"2020071611533060900_R3","author":"Von Recklinghausen","year":"1882","journal-title":"Ueber die multiplen; fibrome der Hautund inhre beziehung zu den multiplen neuromen"},{"key":"2020071611533060900_R4","first-page":"180","article-title":"Recognition of neurofibromatosis before von Recklinghausen.","volume":"2","author":"Hecht","year":"1989","journal-title":"Neurofibromatosis"},{"key":"2020071611533060900_R5","doi-asserted-by":"crossref","first-page":"190","DOI":"10.1097\/00000441-195408000-00008","article-title":"Concomitance of multiple adenomas of the parathyroids and pancreatic islet cells with tumor of the pituitary: a syndrome with familial incidence.","volume":"228","author":"Moldawer","year":"1954","journal-title":"Am J Med Sci"},{"key":"2020071611533060900_R6","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1016\/0002-9343(54)90353-8","article-title":"Genetic aspects of adenomatosis of endocrine glands.","volume":"16","author":"Wermer","year":"1954","journal-title":"Am J Med"},{"key":"2020071611533060900_R7","doi-asserted-by":"crossref","first-page":"371","DOI":"10.1097\/00005792-196809000-00001","article-title":"Study of a kindred with pheochromocytoma, medullary thyroid carcinoma, hyperparathyroidism and Cushing\u2019s disease: multiple endocrine neoplasia, type 2.","volume":"47","author":"Steiner","year":"1968","journal-title":"Medicine (Baltimore)"},{"key":"2020071611533060900_R8","doi-asserted-by":"crossref","first-page":"595","DOI":"10.1016\/0002-9343(64)90107-X","article-title":"Lindau\u2019s disease: review of the literature and study of a large kindred.","volume":"36","author":"Melmon","year":"1964","journal-title":"Am J Med"},{"key":"2020071611533060900_R9","first-page":"534","article-title":"Eye symptoms in tuberous sclerosis of the brain and in Recklinghausen disease.","volume":"45","author":"Van der Hoeve","year":"1923","journal-title":"Trans Ophthalmol Soc UK"},{"key":"2020071611533060900_R10","doi-asserted-by":"crossref","first-page":"530","DOI":"10.1093\/jnci\/92.7.530","article-title":"National Cancer Institute workshop report. 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