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Endocrinology Unit, IRCCS Ospedale Policlinico San Martino, Genoa, Italy
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Pituitary Center Rotterdam, Erasmus MC, Rotterdam, The Netherlands
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Department of Internal Medicine and & Medical Specialties (DIMI) and Center of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy
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Pituitary Center Rotterdam, Erasmus MC, Rotterdam, The Netherlands
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Introduction The presence of an ACTH-secreting pituitary adenoma (corticotroph adenoma) in the anterior or intermediate lobe of the pituitary gland is the cause of Cushing’s disease (CD), a severe systemic condition characterized by a chronic
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ABSTRACT
The presence of immunoreactive (ir)-α-MSH has been investigated by immunocytochemistry in 24 pituitary adenomas and one case of corticotroph hyperplasia causing Cushing's disease, in four adenomas causing Nelson's syndrome, and in ten 'silent' corticotroph adenomas. It was found that a high proportion of these adenomas have a population of cells containing ir-α-MSH in addition to ir-ACTH. In some instances, these adenomas were clearly not associated with the residual intermediate lobe of the pituitary. Radioimmunoassay of plasma from patients with Cushing's disease or Nelson's syndrome showed elevated levels of ir-α-MSH in the majority of cases. Characterization of the ir-α-MSH in adenoma cells by immunocytochemistry, using an antiserum selective for acetylated forms of α-MSH, suggested that only the desacetyl form was present in each case examined. High-performance liquid chromatography of adenoma tissue extracts revealed material co-eluting with acetylated forms of α-MSH in only one of six cases. These results have been compared with corticotroph adenomas in animal pituitary glands, and it is concluded that the presence of α-MSH peptides cannot be used as a marker for intermediate lobe tumours, and that desacetyl α-MSH is commonly produced by corticotroph adenomas.
Journal of Endocrinology (1989) 120, 531–536
Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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Neuromed Institute, IRCCS, Pozzilli, Via Atinense 18, 86077 Pozzilli (IS), Italy
Department of Experimental Medicine and Pathology, University ‘La Sapienza’, Policlinico Umberto 1°, Viale dell’Università, 00161 Rome (RM), Italy
Pathology, S Salvatore Hospital, L’Aquila, Coppito, 67 100 L’Aquila (AQ), Italy
Departments of Neurological Sciences, Policlinico Umberto 1°, Via Regina Margherita, 00161 Roma (RM), Italy
Fondazione ‘Carlo Ferri’, Via E. Riva 42, 00015 Monterotondo (RM), Italy
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differentiation of neuroblastoma cells ( Cho et al. 2001 , Kim et al. 2002 ). In human pituitary tumours, NeuroD1 is expressed by corticotroph adenomas and also by most non-secreting adenomas ( Oyama et al. 2001 , Ferretti et al. 2003 ), with a possible
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the corticotropinoma cells may account for the different response to IFNG on ACTH production, the expression of IFN-γR1 and 2 in corticotroph adenoma tissue was evaluated by immunohistochemistry. IFN-γR1 and 2 expression in human adult normal pituitary
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a gain-of-function mutation in the GNAS ( Landis et al . 1989 ) and USP8 ( Ma et al . 2015 , Reincke et al . 2015 ) genes in a significant proportion of somatotroph and corticotroph adenomas, while amplification in PIK3CA could be a
Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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Health Science Center, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences and Shanghai Second Medical University, Shanghai 200025, People’s Republic of China
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and normal lung lacking POMC expression, whereas hypomethylation was identified in the DMS-79 cell line, bronchial carcinoids and pituitary corticotroph adenoma expressing POMC ( Newell-Price et al. 2001 ). Usually the methylated CpG islands in the
South Australian Adult Genetics Unit, Royal Adelaide Hospital, Adelaide, Australia
Adelaide Medical School, University of Adelaide, Adelaide, Australia
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Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia
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St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia
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Academy for Medical Education, Faculty of Medicine, the University of Queensland, Brisbane, Australia
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Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia
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and mitotic count were retained but with emphasis placed on ‘higher-risk’ histological types: silent corticotroph adenoma, PIT-1 positive plurihormonal adenoma, sparsely granulated somatotroph adenoma, lactotroph adenoma in men and Crooke’s cell
Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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Department of Morphological Sciences, Universidad de Córdoba, Córdoba, Spain
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Service of Endocrinology and Nutrition, Hospital Universitario Reina Sofía, Córdoba, Spain
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Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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Department of Cell Biology, Physiology and Immunology, Universidad de Córdoba, Córdoba, Spain
Hospital Universitario Reina Sofía, Córdoba, Spain
CIBER Fisiopatología de la Obesidad y Nutrición (CIBERObn), Córdoba, Spain
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-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5 . European Journal of Endocrinology 152 645 – 654 . ( doi:10.1530/eje.1.01876 ) Hofland LJ Feelders RA de Herder WW
Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands
Corcept Therapeutics, Menlo Park, CA, USA
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& Laufgraben 2013 ). Previous results in patients with endogenous CS due to pituitary corticotroph adenomas showed that long-term treatment with mifepristone resulted in a continuous elevation of circulating ACTH ( Fleseriu et al. 2014 ), driving subsequent
Department of Biological Pharmacy, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan
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Department of Biological Pharmacy, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan
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Department of Biological Pharmacy, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan
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Department of Biological Pharmacy, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan
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Department of Biological Pharmacy, School of Pharmacy, Shujitsu University, Okayama 703-8516, Japan
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inhibition of ACTH peptides: small cell lung cancer cell lines are more resistant than pituitary corticotroph adenoma cells. Journal of Molecular Endocrinology 10 25 –32. Gagner JP & Drouin J 1985 Opposite