{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T00:48:26Z","timestamp":1790470106615,"version":"4.1.0"},"reference-count":149,"publisher":"The Endocrine Society","issue":"9","license":[{"start":{"date-parts":[[2020,6,29]],"date-time":"2020-06-29T00:00:00Z","timestamp":1593388800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>This review reports the main molecular alterations leading to development of benign cortisol- and\/or aldosterone-secreting adrenal tumors. Causes of adrenal Cushing syndrome can be divided in 2 groups: multiple bilateral tumors or adenomas secreting cortisol. Bilateral causes are mainly primary pigmented nodular adrenocortical disease, most of the time due to PRKAR1A germline-inactivating mutations, and primary bilateral macronodular adrenal hyperplasia that can be caused in some rare syndromic cases by germline-inactivating mutations of MEN1, APC, and FH and of ARMC5 in isolated forms. PRKACA somatic-activating mutations are the main alterations in unilateral cortisol-producing adenomas. In primary hyperaldosteronism (PA), familial forms were identified in 1% to 5% of cases: familial hyperaldosteronism type I (FH-I) due to a chimeric CYP11B1\/CYP11B2 hybrid gene, FH-II due to CLCN-2 germline mutations, FH-III due to KCNJ5 germline mutations, FH-IV due to CACNA1H germline mutations and PA, and seizures and neurological abnormalities syndrome due to CACNA1D germline mutations. Several somatic mutations have been found in aldosterone-producing adenomas in KCNJ5, ATP1A1, ATP2B3, CACNA1D, and CTNNB1 genes.<\/jats:p>\n               <jats:p>In addition to these genetic alterations, genome-wide approaches identified several new alterations in transcriptome, methylome, and miRnome studies, highlighting new pathways involved in steroid dysregulation.<\/jats:p>","DOI":"10.1210\/jendso\/bvaa075","type":"journal-article","created":{"date-parts":[[2020,6,29]],"date-time":"2020-06-29T12:54:25Z","timestamp":1593435265000},"source":"Crossref","is-referenced-by-count":35,"title":["Molecular Basis of Primary Aldosteronism and Adrenal Cushing Syndrome"],"prefix":"10.1210","volume":"4","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3195-1629","authenticated-orcid":false,"given":"Patricia","family":"Vaduva","sequence":"first","affiliation":[{"name":"Reference Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique H\u00f4pitaux de Paris, H\u00f4pital Cochin, Paris, France"},{"name":"Institut Cochin, INSERM U1016, CNRS UMR8104, Paris University, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fideline","family":"Bonnet","sequence":"additional","affiliation":[{"name":"Institut Cochin, INSERM U1016, CNRS UMR8104, Paris University, Paris, France"},{"name":"Hormonal Biology Laboratory, Assistance Publique H\u00f4pitaux de Paris, H\u00f4pital Cochin, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2551-3008","authenticated-orcid":false,"given":"J\u00e9r\u00f4me","family":"Bertherat","sequence":"additional","affiliation":[{"name":"Reference Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique H\u00f4pitaux de Paris, H\u00f4pital Cochin, Paris, France"},{"name":"Institut Cochin, INSERM U1016, CNRS UMR8104, Paris University, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2020,6,29]]},"reference":[{"issue":"1","key":"2020091203140357900_CIT0001","doi-asserted-by":"crossref","first-page":"12","DOI":"10.1111\/j.1365-2265.2011.04253.x","article-title":"Subclinical Cushing\u2019s syndrome: definition and management","volume":"76","author":"Terzolo","year":"2012","journal-title":"Clin Endocrinol (Oxf)."},{"issue":"3","key":"2020091203140357900_CIT0002","doi-asserted-by":"crossref","first-page":"200","DOI":"10.1097\/MED.0000000000000333","article-title":"Diagnosis of a malignant adrenal mass: the role of urinary steroid metabolite profiling","volume":"24","author":"Bancos","year":"2017","journal-title":"Curr Opin Endocrinol Diabetes Obes."},{"issue":"12","key":"2020091203140357900_CIT0003","doi-asserted-by":"crossref","first-page":"3775","DOI":"10.1210\/jc.2011-1565","article-title":"Urine steroid metabolomics as a biomarker tool for detecting malignancy in adrenal tumors","volume":"96","author":"Arlt","year":"2011","journal-title":"J Clin Endocrinol Metab."},{"issue":"3","key":"2020091203140357900_CIT0004","first-page":"826","article-title":"Preclinical Cushing\u2019s syndrome in adrenal \u201cincidentalomas\u201d: comparison with adrenal Cushing\u2019s syndrome","volume":"75","author":"Reincke","year":"1992","journal-title":"J Clin Endocrinol Metab."},{"issue":"2","key":"2020091203140357900_CIT0005","first-page":"637","article-title":"A survey on adrenal incidentaloma in Italy. 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