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Maria Mizamtsidi Department of Endocrinology, Diabetes and Metabolism, Hellenic Red Cross Hospital, Athens, Greece

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Constantinos Nastos Second Department of Surgery, Endocrine Surgery Unit, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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George Mastorakos Unit of Endocrinology, Diabetes and Metabolism, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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Roberto Dina Department of Pathology, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, UK

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Ioannis Vassiliou Second Department of Surgery, Endocrine Surgery Unit, Aretaieion University Hospital, National and Kapodistrian University of Athens, Athens, Greece

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Maria Gazouli Department of Basic Medical Sciences, Laboratory of Biology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece

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Fausto Palazzo Department of Thyroid and Endocrine Surgery, Imperial College London, London, UK

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the emergence of adenomas, hyperplasias and carcinomas ( 5 , 6 ), although it seems that epigenetic changes could also participate actively in parathyroid tumorigenesis ( 7 , 8 ). The main focus of the present study is to present the current optimal

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-17-0283
Volume/Issue:
Volume 7: Issue 2
Open access
Kelly Brewer Center for Molecular Oncology, University of Connecticut School of Medicine, Farmington, Connecticut, USA

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Isabel Nip Center for Molecular Oncology, University of Connecticut School of Medicine, Farmington, Connecticut, USA

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Justin Bellizzi Center for Molecular Oncology, University of Connecticut School of Medicine, Farmington, Connecticut, USA

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Jessica Costa-Guda Center for Molecular Oncology, University of Connecticut School of Medicine, Farmington, Connecticut, USA
Center for Regenerative Medicine and Skeletal Development, Department of Reconstructive Sciences, University of Connecticut School of Dental Medicine, Farmington, Connecticut, USA

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Andrew Arnold Center for Molecular Oncology, University of Connecticut School of Medicine, Farmington, Connecticut, USA
Division of Endocrinology and Metabolism, University of Connecticut School of Medicine, Farmington, Connecticut, USA

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). Approximately 85% of all PHPT cases are caused by sporadic single-gland parathyroid adenomas (PTAs), benign tumors which typically release inappropriately high levels of parathyroid hormone (PTH) and cause hypercalcemia, in turn often leading to osteoporosis

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0055
Volume/Issue:
Volume 10: Issue 3
Open access
Elena Pardi Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Stefano Mariotti Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Natalia S Pellegata Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Katiuscia Benfini Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Simona Borsari Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Federica Saponaro Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Liborio Torregrossa Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Antonello Cappai Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Chiara Satta Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Marco Mastinu Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Claudio Marcocci Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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Filomena Cetani Endocrine Unit 2, Endocrinology Unit, Institute of Pathology, Department of Surgical, Department of Clinical and Experimental Medicine, University Hospital of Pisa, University of Pisa, Via Paradisa 2, Pisa, Italy

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negative result. The search for mutations of other genes involved in parathyroid tumorigenesis allowed the identification of a c.374_375delCT germline mutation in the CDKN1B gene, leading to the diagnosis of MEN4. The age at diagnosis of PHPT in our

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-14-0116
Volume/Issue:
Volume 4: Issue 1
Open access
Luigia Cinque Medical Genetics, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Angelo Sparaneo Laboratory of Oncology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Antonio S Salcuni Endocrinology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Danilo de Martino Thoracic Surgery, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Claudia Battista Endocrinology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Francesco Logoluso Department of Emergency and Organ Transplantation, Unit of Endocrinology, University Medical School of Bari ‘Aldo Moro’, Bari, Italy

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Orazio Palumbo Medical Genetics, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Roberto Cocchi Maxillofacial Surgery, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Evaristo Maiello Oncoematology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Paolo Graziano Pathology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Geoffrey N Hendy Departments of Medicine, Physiology and Human Genetics, McGill University and Metabolic Disorders and Complications, McGill University Health Centre Research Institute, Montreal, Quebec, Canada

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David E C Cole Departments of Laboratory Medicine and Pathobiology, Medicine and Genetics, University of Toronto, Toronto, Ontario, Canada

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Alfredo Scillitani Endocrinology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Vito Guarnieri Medical Genetics, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy

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Introduction The multiple endocrine neoplasia type 1 syndrome (MEN1, MIM131100) is primarily characterized by parathyroid, gastro-entero-pancreatic and pituitary tumors ( 1 , 2 ). Less frequently, it is associated with adrenocortical ( 3

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0207
Volume/Issue:
Volume 6: Issue 8
Open access
Weixi Wang Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Rulai Han Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Lei Ye Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Jing Xie Department of Pathology, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China

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Bei Tao Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Fukang Sun Department of Urology, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China

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Ran Zhuo Department of Urology, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China

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Xi Chen Department of General Surgery, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Xiaxing Deng Pancreatic Disease Centre, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China

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Cong Ye Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China

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Hongyan Zhao Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Shu Wang Shanghai Key Laboratory for Endocrine Tumors, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases and Shanghai E-Institute for Endocrinology, Ruijin Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China

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Introduction Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease characterized by the presence of endocrine tumors mainly affecting parathyroid, pituitary and pancreatic islet. Adrenal lesions occur in 20–55% of MEN1

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0526
Volume/Issue:
Volume 8: Issue 3
Open access
K E Lines
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R P Vas Nunes
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M Frost Academic Endocrine Unit, OCDEM, University of Oxford, Churchill Hospital, Oxford, UK

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C J Yates Academic Endocrine Unit, OCDEM, University of Oxford, Churchill Hospital, Oxford, UK

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M Stevenson Academic Endocrine Unit, OCDEM, University of Oxford, Churchill Hospital, Oxford, UK

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R V Thakker Academic Endocrine Unit, OCDEM, University of Oxford, Churchill Hospital, Oxford, UK

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Introduction Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder, characterised by the combined occurrence of tumours of the parathyroid glands, and neuroendocrine tumours (NETs) of the pancreatic islets and anterior

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0040
Volume/Issue:
Volume 6: Issue 4
Open access
Kate E Lines Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Mahsa Javid Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Anita A C Reed Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Gerard V Walls Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Mark Stevenson Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Michelle Simon MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire, UK

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Kreepa G Kooblall Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Sian E Piret Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Paul T Christie Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Paul J Newey Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Ann-Marie Mallon MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire, UK

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Rajesh V Thakker Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Introduction Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder characterised by the occurrence of parathyroid, pancreatic islet and anterior pituitary tumours. In addition, some patients may also develop adrenal

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-20-0103
Volume/Issue:
Volume 9: Issue 5
Open access
Qianqian Pang Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China
Musculoskeletal Research Laboratory and Bone Quality and Health Assessment Centre, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong

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Yuping Xu Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China
Department of Endocrinology, The First Affiliated Hospital of Shanxi Medical University, Taiyuan, Shanxi, China

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Xuan Qi Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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Yan Jiang Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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Ou Wang Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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Mei Li Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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Xiaoping Xing Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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Ling Qin Musculoskeletal Research Laboratory and Bone Quality and Health Assessment Centre, Department of Orthopedics & Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, Hong Kong

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Weibo Xia Department of Endocrinology, Key Laboratory of Endocrinology, Ministry of Health, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China

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necrosis factor-α (TNF-α) were measured spectrophostometrically using routine assays available at the central laboratory of PUMCH. Serum intact parathyroid hormone (iPTH) and beta- C-terminal telopeptide of type I collagen (β-CTX) were measured by an

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-19-0149
Volume/Issue:
Volume 8: Issue 6
Open access
Anna Gorbacheva Endocrinology Research Center, Moscow, Russian Federation

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Anna Eremkina Endocrinology Research Center, Moscow, Russian Federation

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Daria Goliusova Endocrinology Research Center, Moscow, Russian Federation

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Julia Krupinova Endocrinology Research Center, Moscow, Russian Federation

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Natalia Mokrysheva Endocrinology Research Center, Moscow, Russian Federation

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. In MEN1, lesions of parathyroid glands have the highest penetrance; they manifest with primary hyperparathyroidism (PHPT). Conversely, PHPT is a powerful etiological factor that can lead to bone disorders including the significant decrease in bone

Article Type:
Review Article
Collections:
Hormones and Cancer
DOI:
https://doi.org/10.1530/EC-21-0494
Volume/Issue:
Volume 11: Issue 3
Open access
Francesca Marini Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy
F.I.R.M.O. Italian Foundation for the Research on Bone Diseases, Florence, Italy

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Francesca Giusti Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy

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Teresa Iantomasi Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy

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Federica Cioppi University Hospital of Florence, Azienda Ospedaliero Universitaria Careggi (AOUC), Florence, Italy

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Maria Luisa Brandi F.I.R.M.O. Italian Foundation for the Research on Bone Diseases, Florence, Italy

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-endocrine tissues, caused by germline heterozygote inactivating mutations of the MEN1 tumor-suppressor gene. The main affected organs are parathyroid glands, neuroendocrine cells of the gastro-entero-pancreatic tract (GEP), and the anterior pituitary. Multiple

Article Type:
Research Article
Collections:
Bone and Mineral Metabolism
DOI:
https://doi.org/10.1530/EC-21-0456
Volume/Issue:
Volume 11: Issue 5
Open access