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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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inactivating mutations of the MEN1 gene, encoding menin, an intracellular protein that interacts with transcription factors involved in cell cycle regulation and proliferation ( 8 ). Fifteen well-documented cases of parathyroid carcinoma (PC) and one atypical

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Sara Lomelino Pinheiro Serviço de Endocrinologia, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Ana Saramago Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Branca Maria Cavaco Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Carmo Martins Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Valeriano Leite Serviço de Endocrinologia e Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Tiago Nunes da Silva Serviço de Endocrinologia e Unidade de Investigação em Patobiologia Molecular, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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hyperparathyroidism (FIHP; CDC73/HRPT2 and GCM2 genes) and, rarely, in multiple endocrine neoplasia type 1 (MEN1, MEN1 gene) and 2A (MEN2A; RET gene) ( 2 , 3 ). MEN1 is a rare disorder characterized by PHPT, pituitary and gastroenteropancreatic

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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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, inheritance and prognosis of ACC associated with MEN1 remain unclear. The molecular pathogenesis of ACC has been associated with the tumor suppressor gene TP53 . An unusually high incidence of ACC has been found in children in southern Brazil and a founder

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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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pituitary (1) . MEN1 is caused by heterozygous germline mutations of the MEN1 gene, and tumours developed by MEN1 patients show loss of the remaining normal copy of the MEN1 gene, a ‘second-hit’, demonstrating the tumour suppressor function of its

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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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cortical tumours, carcinoids, facial angiofibromas, collagenomas and lipomas ( 1 ). MEN1-associated tumours show a loss of heterozygosity of the MEN1 gene, which is located on chromosome 11q13 and encodes the ubiquitously expressed, predominantly nuclear

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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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gene – the main molecular defect causing the MEN1 syndrome – have been detected in about 70–80% and 30% of patients with familial and sporadic MEN1 respectively (3) . The percentage in familial MEN1 rises to 90% if a search for large germline deletions

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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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Introduction Menin is a highly conserved protein encoded by the ubiquitously expressed MEN1 gene. It partakes in the regulation of various intracellular processes, including transcription, maintaining genome stability, proliferation and

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Elizaveta Mamedova Department of Neuroendocrinology and Bone Diseases, Endocrinology Research Center, Moscow, Russian Federation

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Natalya Mokrysheva Department of Parathyroid Diseases, Endocrinology Research Center, Moscow, Russian Federation

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Evgeny Vasilyev Department and Laboratory of Inherited Endocrine Disorders, Endocrinology Research Center, Moscow, Russian Federation

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Vasily Petrov Department and Laboratory of Inherited Endocrine Disorders, Endocrinology Research Center, Moscow, Russian Federation

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Ekaterina Pigarova Department of Neuroendocrinology and Bone Diseases, Endocrinology Research Center, Moscow, Russian Federation

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Sergey Kuznetsov Department of Surgery, Endocrinology Research Center, Moscow, Russian Federation

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Nikolay Kuznetsov Department of Surgery, Endocrinology Research Center, Moscow, Russian Federation

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Liudmila Rozhinskaya Department of Neuroendocrinology and Bone Diseases, Endocrinology Research Center, Moscow, Russian Federation

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Galina Melnichenko I.M. Sechenov First Moscow State Medical University, Moscow, Russian Federation
Institute of Clinical Endocrinology, Endocrinology Research Center, Moscow, Russian Federation

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Ivan Dedov Endocrinology Research Center, Moscow, Russian Federation

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Anatoly Tiulpakov Department and Laboratory of Inherited Endocrine Disorders, Endocrinology Research Center, Moscow, Russian Federation

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55 patients. A custom-designed panel included genes associated or presumably associated with familial forms of PHPT, except MEN2A and FHH types 2 and 3: MEN1 , CASR , CDC73 , CDKN1A , CDKN1B , CDKN1C , CDKN2A , CDKN2C and CDKN2D . Primers

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Debra M Gordon University of the Witwatersrand (WITS) Donald Gordon Medical Centre, Parktown, Johannesburg, South Africa

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Pablo Beckers Department of Human Genetics, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Emilie Castermans Department of Human Genetics, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Sebastian J C M M Neggers Department of Endocrinology, Erasmus University Medical Center, Rotterdam, The Netherlands

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Liliya Rostomyan Department of Endocrinology, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Vincent Bours Department of Human Genetics, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Patrick Petrossians Department of Endocrinology, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Vinciane Dideberg Department of Human Genetics, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Albert Beckers Department of Endocrinology, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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Adrian F Daly Department of Endocrinology, Centre Hospitalier Universitaire de Liège, Liège Université, Liège, Belgium

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sequencing for genes of interest: multiplex ligand-dependent probe amplification (MLPA) was used to assess for the presence of whole or partial gene deletions. The panel of genes assessed included: AIP , MEN1 , CDKN1B , SDHA, SDHB, SDHC, SDHD, SDHAF2, VHL

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K L Gatford School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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G K Heinemann School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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S D Thompson School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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J V Zhang School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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S Buckberry School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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J A Owens School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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G A Dekker School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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C T Roberts School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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on behalf of the SCOPE Consortium School of Paediatrics and Reproductive Health, Robinson Research Institute, University of Adelaide, Adelaide, South Australia 5005, Australia

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– 434 . ( doi:10.1203/PDR.0b013e3181f1ca99 ). 51 Heude B Ong KK Luben R Wareham NJ Sandhu MS . Study of association between common variation in the insulin-like growth factor 2 gene and indices of obesity and body size in middle-aged men and

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