{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:20:30Z","timestamp":1784557230590,"version":"3.55.0"},"reference-count":172,"publisher":"Bioscientifica","issue":"10","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,10]]},"abstract":"\n The identification of the multiple endocrine neoplasia type 1 (\n MEN1<\/jats:italic>\n ) gene in 1997 has shown that germline heterozygous mutations in the\n MEN1<\/jats:italic>\n gene located on chromosome 11q13 predisposes to the development of tumors in the MEN1 syndrome. Tumor development occurs upon loss of the remaining normal copy of the\n MEN1<\/jats:italic>\n gene in MEN1-target tissues. Therefore,\n MEN1<\/jats:italic>\n is a classic tumor suppressor gene in the context of MEN1. This tumor suppressor role of the protein encoded by the\n MEN1<\/jats:italic>\n gene, menin, holds true in mouse models with germline heterozygous\n Men1<\/jats:italic>\n loss, wherein MEN1-associated tumors develop in adult mice after spontaneous loss of the remaining non-targeted copy of the\n Men1<\/jats:italic>\n gene. The availability of genetic testing for mutations in the\n MEN1<\/jats:italic>\n gene has become an essential part of the diagnosis and management of MEN1. Genetic testing is also helping to exclude mutation-negative cases in MEN1 families from the burden of lifelong clinical screening. In the past 20 years, efforts of various groups world-wide have been directed at mutation analysis, molecular genetic studies, mouse models, gene expression studies, epigenetic regulation analysis, biochemical studies and anti-tumor effects of candidate therapies in mouse models. This review will focus on the findings and advances from these studies to identify\n MEN1<\/jats:italic>\n germline and somatic mutations, the genetics of MEN1-related states, several protein partners of menin, the three-dimensional structure of menin and menin-dependent target genes. The ongoing impact of all these studies on disease prediction, management and outcomes will continue in the years to come.\n <\/jats:p>","DOI":"10.1530\/erc-17-0199","type":"journal-article","created":{"date-parts":[[2017,9,12]],"date-time":"2017-09-12T20:40:18Z","timestamp":1505248818000},"page":"T119-T134","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-8","source":"Crossref","is-referenced-by-count":86,"title":["The future: genetics advances in MEN1 therapeutic approaches and management strategies"],"prefix":"10.1530","volume":"24","author":[{"given":"Sunita K","family":"Agarwal","sequence":"first","affiliation":[{"name":"Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Frontiers in Hormone Research","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1159\/000345666","article-title":"Multiple endocrine neoplasia type 1","volume":"41","author":"Agarwal","year":"2013","unstructured":"Agarwal SK 2013 Multiple endocrine neoplasia type 1. 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