{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T01:45:32Z","timestamp":1783647932102,"version":"3.55.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2024,2,1]],"date-time":"2024-02-01T00:00:00Z","timestamp":1706745600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001665","name":"Agence Nationale de la Recherche","doi-asserted-by":"publisher","award":["ANR-18-CE14-0021 INTE-GRAL"],"award-info":[{"award-number":["ANR-18-CE14-0021 INTE-GRAL"]}],"id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001677","name":"Inserm","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001677","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002738","name":"AP-HP","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>A paradoxical increase of growth hormone (GH) following oral glucose load has been described in \u223c30% of patients with acromegaly and has been related to the ectopic expression of the glucose-dependent insulinotropic polypeptide (GIP) receptor (GIPR) in somatotropinomas. Recently, we identified germline pathogenic variants and somatic loss of heterozygosity of lysine demethylase 1A (KDM1A) in patients with GIP-dependent primary bilateral macronodular adrenal hyperplasia with Cushing's syndrome. The ectopic expression of GIPR in both adrenal and pituitary lesions suggests a common molecular mechanism.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>We aimed to analyze KDM1A gene sequence and KDM1A and GIPR expressions in somatotroph pituitary adenomas.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Settings<\/jats:title>\n                  <jats:p>We conducted a cohort study at university hospitals in France and in Italy. We collected pituitary adenoma specimens from acromegalic patients who had undergone pituitary surgery. We performed targeted exome sequencing (gene panel analysis) and array-comparative genomic hybridization on somatic DNA derived from adenomas and performed droplet digital PCR on adenoma samples to quantify KDM1A and GIPR expressions.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>One hundred and forty-six patients with sporadic acromegaly were studied; 72.6% presented unsuppressed classical GH response, whereas 27.4% displayed a paradoxical rise in GH after oral glucose load. We did not identify any pathogenic variant in the KDM1A gene in the adenomas of these patients. However, we identified a recurrent 1p deletion encompassing the KDM1A locus in 29 adenomas and observed a higher prevalence of paradoxical GH rise (P = .0166), lower KDM1A expression (4.47 \u00b1 2.49 vs 8.56 \u00b1 5.62, P &amp;lt; .0001), and higher GIPR expression (1.09 \u00b1 0.92 vs 0.43 \u00b1 0.51, P = .0012) in adenomas from patients with KDM1A haploinsufficiency compared with those with 2 KDM1A copies.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions and relevance<\/jats:title>\n                  <jats:p>Unlike in GIP-dependent primary bilateral macronodular adrenal hyperplasia, KDM1A genetic variations are not the cause of GIPR expression in somatotroph pituitary adenomas. Recurrent KDM1A haploinsufficiency, more frequently observed in GIPR-expressing adenomas, could be responsible for decreased KDM1A function resulting in transcriptional derepression on the GIPR locus.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ejendo\/lvae013","type":"journal-article","created":{"date-parts":[[2024,2,8]],"date-time":"2024-02-08T19:19:21Z","timestamp":1707419961000},"page":"173-181","source":"Crossref","is-referenced-by-count":13,"title":["<i>KDM1A<\/i> genotyping and expression in 146 sporadic somatotroph pituitary adenomas"],"prefix":"10.1093","volume":"190","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2228-9437","authenticated-orcid":false,"given":"Fanny","family":"Chasseloup","sequence":"first","affiliation":[{"name":"Inserm, Universit\u00e9 Paris-Saclay, Physiologie et Physiopathologie Endocriniennes, AP-HP, H\u00f4pital Bic\u00eatre, Service d\u2019Endocrinologie et des Maladies de la Reproduction, Centre de R\u00e9f\u00e9rence des Maladies Rares de l\u2019Hypophyse , 94270 Le Kremlin-Bic\u00eatre , France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1942-7202","authenticated-orcid":false,"given":"Daniela","family":"Regazzo","sequence":"additional","affiliation":[{"name":"Department of Medicine, Endocrinology Unit, University of Padova , 35128 Padova , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucie","family":"Tosca","sequence":"additional","affiliation":[{"name":"AP-HP, H\u00f4pital Antoine B\u00e9cl\u00e8re, Universit\u00e9 Paris-Saclay, Service d\u2019Histologie, Embryologie et Cytog\u00e9nomique , 92140 Clamart , France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexis","family":"Proust","sequence":"additional","affiliation":[{"name":"AP-HP, H\u00f4pital Bic\u00eatre, Service de G\u00e9n\u00e9tique Mol\u00e9culaire et d\u2019Hormonologie , 94270 Le Kremlin Bic\u00eatre , 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