{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T17:29:23Z","timestamp":1790270963268,"version":"4.1.0"},"reference-count":84,"publisher":"Bioscientifica","issue":"10","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:p>\n                    Multiple endocrine neoplasia (MEN) refers to a group of autosomal dominant disorders with generally high penetrance that lead to the development of a wide spectrum of endocrine and non-endocrine manifestations. The most frequent among these conditions is MEN type 1 (MEN1), which is caused by germline heterozygous loss-of-function mutations in the tumor suppressor gene\n                    <jats:italic>MEN1<\/jats:italic>\n                    . MEN1 is characterized by primary hyperparathyroidism (PHPT) and functional or nonfunctional pancreatic neuroendocrine tumors and pituitary adenomas. Approximately 10% of patients with familial or sporadic MEN1-like phenotype do not have\n                    <jats:italic>MEN1<\/jats:italic>\n                    mutations or deletions. A novel MEN syndrome was discovered, initially in rats (MENX), and later in humans (MEN4), which is caused by germline mutations in the putative tumor suppressor\n                    <jats:italic>CDKN1B<\/jats:italic>\n                    . The most common phenotype of the 19 established cases of MEN4 that have been described to date is PHPT followed by pituitary adenomas. Recently, somatic or germline mutations in\n                    <jats:italic>CDKN1B<\/jats:italic>\n                    were also identified in patients with sporadic PHPT, small intestinal neuroendocrine tumors, lymphoma and breast cancer, demonstrating a novel role for\n                    <jats:italic>CDKN1B<\/jats:italic>\n                    as a tumor susceptibility gene for other neoplasms. In this review, we report on the genetic characterization and clinical features of MEN4.\n                  <\/jats:p>","DOI":"10.1530\/erc-17-0243","type":"journal-article","created":{"date-parts":[[2017,8,19]],"date-time":"2017-08-19T20:10:16Z","timestamp":1503173416000},"page":"T195-T208","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-8","source":"Crossref","is-referenced-by-count":175,"title":["MEN4 and CDKN1B mutations: the latest of the MEN syndromes"],"prefix":"10.1530","volume":"24","author":[{"given":"Rami","family":"Alrezk","sequence":"first","affiliation":[{"name":"The National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fady","family":"Hannah-Shmouni","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Constantine A","family":"Stratakis","sequence":"additional","affiliation":[{"name":"Section on Endocrinology & Genetics, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Human Molecular Genetics","first-page":"1169","article-title":"Germline mutations of the MEN1 gene in familial multiple endocrine neoplasia type 1 and related states","volume":"6","author":"Agarwal","year":"1997","unstructured":"Agarwal SK Kester MB Debelenko LV Heppner C Emmert-Buck MR Skarulis MC Doppman JL Kim YS Lubensky IA Zhuang Z 1997 Germline mutations of the MEN1 gene in familial multiple endocrine neoplasia type 1 and related states. 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