{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,23]],"date-time":"2026-05-23T09:09:35Z","timestamp":1779527375440,"version":"3.53.1"},"reference-count":216,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["FOC"],"published-print":{"date-parts":[[2015,2]]},"abstract":"\n OBJECT<\/jats:title>\n Functional corticotroph pituitary adenomas (PAs) secrete adrenocorticotropic hormone (ACTH) and are the cause of Cushing's disease, which accounts for 70% of all cases of Cushing's syndrome. Current classification systems for PAs rely primarily on laboratory hormone findings, tumor size and morphology, invasiveness, and immunohistochemical findings. Likewise, drug development for functional ACTH-secreting PAs (ACTH-PAs) is limited and has focused largely on blocking the production or downstream effects of excess cortisol. The authors aimed to summarize the findings from previous studies that explored gene and protein expression of ACTH-PAs to prioritize potential genetic and protein targets for improved molecular diagnosis and treatment of Cushing's disease.<\/jats:p>\n <\/jats:sec>\n \n METHODS<\/jats:title>\n A systematic literature review was performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A PubMed search of select medical subject heading (MeSH) terms was performed to identify all studies that reported gene- and protein-expression findings in ACTH-PAs from January 1, 1990, to August 24, 2014, the day the search was performed. The inclusion criteria were studies on functional ACTH-PAs compared with normal pituitary glands, on human PA tissue only, with any method of analysis, and published in the English language. Studies using anything other than resected PA tissue, those that compared other adenoma types, those without baseline expression data, or those in which any pretreatment was delivered before analysis were excluded.<\/jats:p>\n <\/jats:sec>\n \n RESULTS<\/jats:title>\n \n The primary search returned 1371 abstracts, of which 307 were found to be relevant. Of those, 178 were selected for secondary full-text analysis. Of these, 64 articles met the inclusion criteria and an additional 4 studies were identified from outside the search for a total of 68 included studies. Compared with the normal pituitary gland, significant gene overexpression in 43 genes and 22 proteins was reported, and gene underexpression in 58 genes and 15 proteins was reported. Immunohistochemistry was used in 39 of the studies, and reverse transcriptase polymerase chain reaction was used in 26 of the studies, primarily, and as validation for 4 others. Thirteen studies used both immunohistochemistry and reverse transcriptase polymerase chain reaction. Other methods used included microarray, in situ hybridization, Northern blot analysis, and Western blot analysis. Expression of prioritized genes emphasized in multiple studies were often validated on both the gene and protein levels. Genes\/proteins found to be overexpressed in ACTH-PAs relative to the normal pituitary gland included\n hPTTG1<\/jats:italic>\n \/securin,\n NEUROD1<\/jats:italic>\n \/NeuroD1 (Beta2),\n HSD11B2<\/jats:italic>\n \/11\u03b2-hydroxysteroid dehydrogenase 2,\n AKT<\/jats:italic>\n \/Akt, protein kinase B, and\n CCND1<\/jats:italic>\n \/cyclin D1. Candidate genes\/proteins found to be underexpressed in ACTH-PAs relative to the normal pituitary gland included\n CDKN1B<\/jats:italic>\n \/p27\n Kip1<\/jats:sup>\n ,\n CDKN2A<\/jats:italic>\n \/p16,\n KISS1<\/jats:italic>\n \/kisspeptin,\n ACTHR<\/jats:italic>\n \/ACTH-R, and miR-493.\n <\/jats:p>\n <\/jats:sec>\n \n CONCLUSIONS<\/jats:title>\n On the basis of the authors' systematic review, many significant gene and protein targets that may contribute to tumorigenesis, invasion, and hormone production\/secretion of ACTH have been identified and validated in ACTH-PAs. Many of these potential targets have not been fully analyzed for their therapeutic and diagnostic potential but may represent candidate molecular targets for biomarker development and drug targeting. This review may help catalyze additional research efforts using modern profiling and sequencing techniques and alteration of gene expression.<\/jats:p>\n <\/jats:sec>","DOI":"10.3171\/2014.10.focus14683","type":"journal-article","created":{"date-parts":[[2015,2,1]],"date-time":"2015-02-01T03:40:53Z","timestamp":1422762053000},"page":"E17","source":"Crossref","is-referenced-by-count":26,"title":["Gene and protein expression in pituitary corticotroph adenomas: a systematic review of the literature"],"prefix":"10.3171","volume":"38","author":[{"given":"Justin","family":"Seltzer","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles E.","family":"Ashton","sequence":"additional","affiliation":[{"name":"Zilka Neurogenetics Institute,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas C.","family":"Scotton","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dhiraj","family":"Pangal","sequence":"additional","affiliation":[{"name":"Zilka Neurogenetics Institute,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John D.","family":"Carmichael","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Department of Medicine, Keck School of Medicine of USC, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel","family":"Zada","sequence":"additional","affiliation":[{"name":"Zilka Neurogenetics Institute,"},{"name":"Department of Neurosurgery, and"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1-focus14683","series-title":"Pathol Res Pract","first-page":"541","article-title":"Immunohistochemical demonstration of insulin-like growth factor I (IGF-1) in normal and pathological human pituitary 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tumors","volume":"86","author":"Korbonits","year":"2001"},{"key":"b39-focus14683","series-title":"J Clin Endocrinol Metab","first-page":"3624","article-title":"Expression of the growth hormone secretagogue receptor in pituitary adenomas and other neuroendocrine tumors","volume":"83","author":"Korbonits","year":"1998"},{"key":"b40-focus14683","series-title":"J Biol Chem","first-page":"34631","article-title":"The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54","volume":"276","author":"Kotani","year":"2001"},{"key":"b41-focus14683","series-title":"J Clin Endocrinol Metab","first-page":"1864","article-title":"Endothelin expression in normal human anterior pituitaries and pituitary adenomas","volume":"79","author":"Lange","year":"1994"},{"key":"b42-focus14683","series-title":"World Neurosurg","first-page":"563","article-title":"Results of immunohistochemical staining of cell-cycle regulators: the prediction of recurrence of functioning pituitary adenoma","volume":"81","author":"Lee","year":"2014"},{"key":"b43-focus14683","series-title":"J Endocrinol Invest","first-page":"781","article-title":"Multiple endocrine neoplasia syndromes associated with mutation of p27","volume":"36","author":"Lee","year":"2013"},{"key":"b44-focus14683","series-title":"Oncol Res","first-page":"129","article-title":"MicroRNA-200c inhibits apoptosis in pituitary adenoma cells by targeting the PTEN\/Akt signaling pathway","volume":"21","author":"Liao","year":"2013"},{"key":"b45-focus14683","series-title":"J Clin Endocrinol Metab","first-page":"3823","article-title":"Low expression of the cell cycle inhibitor p27Kip1 in normal corticotroph cells, corticotroph tumors, and malignant pituitary tumors","volume":"84","author":"Lidhar","year":"1999"},{"key":"b46-focus14683","series-title":"Am J Pathol","first-page":"401","article-title":"Aberrant p27kip1 expression in endocrine and other tumors","volume":"150","author":"Lloyd","year":"1997"},{"key":"b47-focus14683","series-title":"Eur J Endocrinol","first-page":"335","article-title":"Association between the p27 rs2066827 variant and tumor multiplicity in patients harboring MEN1 germline mutations","volume":"171","author":"Longuini","year":"2014"},{"key":"b48-focus14683","series-title":"Nat Genet","first-page":"323","article-title":"Mutations in NEUROD1 are associated with the development of type 2 diabetes mellitus","volume":"23","author":"Malecki","year":"1999"},{"key":"b49-focus14683","series-title":"Eur J Endocrinol","first-page":"355","article-title":"Expression of functional KISS1 and KISS1R system is altered in human pituitary adenomas: evidence for apoptotic action of kisspeptin-10","volume":"164","author":"Mart\u00ednez-Fuentes","year":"2011"},{"key":"b50-focus14683","series-title":"Clin Endocrinol (Oxf)","first-page":"727","article-title":"Increased MEN1 mRNA expression in sporadic pituitary tumours","volume":"50","author":"McCabe","year":"1999"},{"key":"b51-focus14683","series-title":"Clin Endocrinol (Oxf)","first-page":"141","article-title":"Expression of pituitary tumour transforming gene (PTTG) and fibroblast growth factor-2 (FGF-2) in human pituitary adenomas: relationships to clinical tumour behaviour","volume":"58","author":"McCabe","year":"2003"},{"key":"b52-focus14683","series-title":"MicroRNA 493 [Homo sapiens (human)]"},{"key":"b53-focus14683","series-title":"Endocr Pathol","first-page":"143","article-title":"PTTG overexpression is correlated with angiogenesis in human pituitary adenomas","volume":"17","author":"Minematsu","year":"2006"},{"key":"b54-focus14683","series-title":"Int J Surg","first-page":"336","article-title":"Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement","volume":"8","author":"Moher","year":"2010"},{"key":"b55-focus14683","series-title":"J Clin Endocrinol Metab","first-page":"6080","article-title":"Identification of adrenocorticotropin receptor messenger ribonucleic acid in the human pituitary and its loss of expression in pituitary adenomas","volume":"88","author":"Morris","year":"2003"},{"key":"b56-focus14683","series-title":"Mol Cell Endocrinol","first-page":"37","article-title":"Inhibitory effects of SOM230 on adrenocorticotropic hormone production and corticotroph tumor cell proliferation in vitro and in vivo","volume":"394","author":"Murasawa","year":"2014"},{"key":"b57-focus14683","series-title":"Endocr Relat Cancer","first-page":"423","article-title":"Enhanced protein kinase B\/Akt signalling in pituitary tumours","volume":"12","author":"Musat","year":"2005"},{"key":"b58-focus14683","series-title":"J Clin Endocrinol Metab","first-page":"1526","article-title":"The diagnosis of Cushing's syndrome: an Endocrine Society Clinical Practice 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