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Medicover Neuroendocrinology, Munich, Germany
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tumours carry somatic mutations in the ubiquitin-specific protease 8 ( USP8 ) gene ( Ma et al. 2015 , Perez-Rivas et al. 2015 , Reincke et al. 2015 , reviewed in Sbiera et al. 2019 ). Studies reported USP8- mutant tumours to be smaller in size
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Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Neurosurgery Unit, Milan, Italy
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Department of Biomedical Sciences, Humanitas University, Milan, Italy
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Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Endocrinology Unit, Milan, Italy
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Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Endocrinology Unit, Milan, Italy
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identification of gain-of-function somatic mutations in the USP8 gene showing a peculiar specificity for corticotropinomas ( Reincke et al. 2015 ). In this context, USP8 mutations lead to enhanced deubiquitination of EGF receptor (EGFR) and consequent
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Department of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany
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Department of Endocrinology, Max Planck Institute of Psychiatry, Munich, Germany
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treatment ( Terzolo et al. 2001 ). The mechanisms underlying the ectopic production of ACTH are still not well understood. Recently, we and others have reported that the gene coding for the human ubiquitin-specific protease 8 ( USP8 ) is recurrently
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Endocrinology Training Programs, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, Maryland, USA
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Endocrinology Training Programs, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, Maryland, USA
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Endocrinology Training Programs, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Bethesda, Maryland, USA
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-Price 2009 ). Although germline mutations in genes such as MEN1 , CDKIs, and AIP , and somatic mutations in USP8 have been identified in patients with CD, for many corticotropinomas the molecular pathways involved in their pathogenesis remain unknown
Inserm U1016, CNRS UMR 8104, Institut Cochin, Université Paris Descartes-Université de Paris, Paris, France
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Department of Neurosurgery, Hôpital Universitaire Pitié-Salpêtrière, APHP, Sorbonne Université, Paris, France
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Department of Endocrinology, Center for Rare Adrenal Diseases, Hôpital Cochin APHP, Paris, France
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Lyon 1 University, Villeurbanne, France
Inserm U1052, CNRS UMR 5286, Cancer Research Center of Lyon, Lyon, France
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USP8 status ( Reincke et al. 2015 , Neou et al. 2020 ), and two subtypes of somatotroph tumours exist when combining transcriptome and GNAS status ( Spada et al. 1990 , Neou et al. 2020 ), which respectively show ubiquitous TPIT and PIT1
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tumors are often more subtle, and although not silent, have been described as ‘whispering’ ( Asa 2011 ). Mutations in the ubiquitin-specific peptidase USP8 ( Ma et al. 2015 , Reincke et al. 2015 , Hayashi et al. 2016 ) have been identified in
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Service of Endocrinology and Nutrition, Hospital Universitario Central de Asturias, Instituto Universitario de Oncología del Principado de Asturias, Universidad de Oviedo, Oviedo, Spain
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Department of Neurosurgery, Hôpital Foch, Suresnes, France
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Service d’Endocrinologie, Cochin Hospital, Assistance Publique Hôpitaux de Paris, Paris, France
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Service d’Endocrinologie, Cochin Hospital, Assistance Publique Hôpitaux de Paris, Paris, France
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Department of Pathological Cytology and Anatomy, Hôpital Foch, Suresnes, France
Department of Endocrinology, CHU de Liège, University of Liège, Liège, Belgium
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, the germline abnormalities leading to corticotroph cell tumorigenesis remain largely unknown. On the other hand, somatic mutations in the USP8 gene hotspot are highly prevalent among corticotropinomas in adult and pediatric patients, but they have
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Department of Endocrinology, APHP, Cochin Hospital, Paris, France
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, recent studies highlight the growing evidences of the ubiquitination/proteasome system alterations in endocrine and more specifically adrenal and pituitary tumors causing Cushing syndrome development. While the ubiquitin-specific protease 8 (USP8) gene is
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Division of Translational and Experimental Medicine, University of Warwick Medical School, Clinical Sciences Research Laboratories, Coventry, UK
Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK
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therapy for ACTH-adenomas, demonstrating promising in vitro results ( Fukuoka et al. 2011 ). Recently, an exhaustive exome-wide screening has led to the identification of somatic mutations in the ubiquitin-specific protease 8 (USP8) in ACTH
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promote lysosomal degradation of MET through interaction of the LRIG1–MET complex with HRS. Furthermore, LRIG1 was identified to be a target of the deubiquitinating enzyme USP8, which was shown to counteract LRIG1 ubiquitination and degradation