{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T08:08:41Z","timestamp":1790842121305,"version":"4.1.0"},"reference-count":38,"publisher":"The Endocrine Society","issue":"5","funder":[{"DOI":"10.13039\/501100002915","name":"Fondation de la Recherche M\u00e9dicale","doi-asserted-by":"crossref","award":["FDM20150632800"],"award-info":[{"award-number":["FDM20150632800"]}],"id":[{"id":"10.13039\/501100002915","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Contrat d\u2019Interface Inserm."}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Besides GNAS gene mutations, the molecular pathogenesis of somatotroph adenomas responsible for gigantism and acromegaly remains elusive.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To investigate alternative driver events in somatotroph tumorigenesis, focusing on a subgroup of acromegalic patients with a paradoxical increase in growth hormone (GH) secretion after oral glucose, resulting from ectopic glucose-dependent insulinotropic polypeptide receptor (GIPR) expression in their somatotropinomas.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Design, Setting, and Patients<\/jats:title>\n                  <jats:p>We performed combined molecular analyses, including array-comparative genomic hybridization, RNA\/DNA fluorescence in situ hybridization, and RRBS DNA methylation analysis on 41 somatotropinoma samples from 38 patients with acromegaly and three sporadic giants. Ten patients displayed paradoxical GH responses to oral glucose.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>GIPR expression was detected in 13 samples (32%), including all 10 samples from patients with paradoxical GH responses. All GIPR-expressing somatotropinomas were negative for GNAS mutations. GIPR expression occurred through transcriptional activation of a single allele of the GIPR gene in all GIPR-expressing samples, except in two tetraploid samples, where expression occurred from two alleles per nucleus. In addition to extensive 19q duplications, we detected in four samples GIPR locus microamplifications in a certain proportion of nuclei. We identified an overall hypermethylator phenotype in GIPR-expressing samples compared with GNAS-mutated adenomas. In particular, we observed hypermethylation in the GIPR gene body, likely driving its ectopic expression.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>We describe a distinct molecular subclass of somatotropinomas, clinically revealed by a paradoxical increase of GH to oral glucose related to pituitary GIPR expression. This ectopic GIPR expression occurred through hypomorphic transcriptional activation and is likely driven by GIPR gene microamplifications and DNA methylation abnormalities.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/jc.2018-01504","type":"journal-article","created":{"date-parts":[[2018,10,29]],"date-time":"2018-10-29T18:03:14Z","timestamp":1540836194000},"page":"1777-1787","source":"Crossref","is-referenced-by-count":41,"title":["Hypermethylator Phenotype and Ectopic GIP Receptor in GNAS Mutation-Negative Somatotropinomas"],"prefix":"10.1210","volume":"104","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7458-7102","authenticated-orcid":false,"given":"Mirella","family":"Hage","sequence":"first","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Le Kremlin Bic\u00eatre, France"},{"name":"Universit\u00e9 Paris-Sud, Universit\u00e9 Paris-Saclay, Le Kremlin-Bic\u00eatre, France"},{"name":"Assistance Publique-H\u00f4pitaux de Paris, Service d\u2019Endocrinologie et des Maladies de la Reproduction, H\u00f4pital de Bic\u00eatre, Centre de R\u00e9f\u00e9rence des Maladies Rares de l\u2019Hypophyse, Le Kremlin-Bic\u00eatre, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronan","family":"Chalign\u00e9","sequence":"additional","affiliation":[{"name":"Division of Hematology and Medical Oncology, Department of Medicine and Meyer Cancer Center, Weill Cornell Medicine, New York, New York"},{"name":"New York Genome Center, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Say","family":"Viengchareun","sequence":"additional","affiliation":[{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Le Kremlin Bic\u00eatre, France"},{"name":"Universit\u00e9 Paris-Sud, Universit\u00e9 Paris-Saclay, Le Kremlin-Bic\u00eatre, 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Paris, Service de G\u00e9n\u00e9tique Mol\u00e9culaire, Pharmacog\u00e9n\u00e9tique et Hormonologie, Le Kremlin-Bic\u00eatre, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Letouz\u00e9","sequence":"additional","affiliation":[{"name":"Unit\u00e9 Mixte de Recherche S1162, \u201cG\u00e9nomique fonctionnelle des tumeurs solides,\u201d Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucie","family":"Tosca","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris-Sud, Universit\u00e9 Paris-Saclay, Le Kremlin-Bic\u00eatre, France"},{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Unit\u00e9 Mixte de Recherche, Fontenay-aux-Roses, France"},{"name":"Assistance Publique-H\u00f4pitaux de Paris, H\u00f4pital Antoine B\u00e9cl\u00e8re, Service d\u2019Histologie-Embryologie-Cytog\u00e9n\u00e9tique, Clamart, 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