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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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genetic alterations associated with sporadic PC are inactivating somatic mutations of the CDC73/HRPT2 gene. Sporadic PC may also be associated with other abnormalities, including p53 and retinoblastoma gene mutations. Alterations of the PI3K

Article Type:
Research Article
Collections:
Bone and Mineral Metabolism
DOI:
https://doi.org/10.1530/EC-22-0479
Volume/Issue:
Volume 12: Issue 9
Open access
Sara Ahmadi Division of Endocrinology, Thyroid Section, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Iñigo Landa Division of Endocrinology, Thyroid Section, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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gain Alterations in RBM10 , SWI/SNF members and chromosome 1q are enriched in nonresponders to RAI (compared to exceptional responders) Bikas et al. 2023 ( 17 ) PTC + FTC, RAS mutant 69 TERT promoter, PTEN , SWI/SNF genes, others

Article Type:
Review Article
Collections:
Thyroid
DOI:
https://doi.org/10.1530/EC-23-0297
Volume/Issue:
Volume 13: Issue 2
Open access
Lukas Ochsner Ridder Department of Endocrinology and Internal Medicine and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark
Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark

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Agnethe Berglund Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Department of Clinical Genetics and Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark

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Kirstine Stochholm Department of Endocrinology and Internal Medicine and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark

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Simon Chang Department of Endocrinology and Internal Medicine and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark
Unit for Thrombosis Research, Hospital of South West Jutland and University of Southern Denmark, Esbjerg, Denmark

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Claus H Gravholt Department of Endocrinology and Internal Medicine and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark
Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark
Unit for Thrombosis Research, Hospital of South West Jutland and University of Southern Denmark, Esbjerg, Denmark

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Introduction Klinefelter syndrome (KS) and 47,XYY syndrome are two distinct common sex chromosome abnormalities sharing some known similarities. KS is comparatively well described, where plentiful studies have expanded our knowledge during

Article Type:
Review Article
Collections:
Reproduction
DOI:
https://doi.org/10.1530/EC-23-0024
Volume/Issue:
Volume 12: Issue 5
Open access
Katherine U Gaynor Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK

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Irina V Grigorieva Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK

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Samantha M Mirczuk Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, 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, Churchill Hospital, Oxford, 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, Churchill Hospital, 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, Churchill Hospital, Oxford, UK

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Karine Rizzoti The Francis Crick Institute, London, UK

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Michael R Bowl Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, Oxford, UK

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M Andrew Nesbit Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, 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, Churchill Hospital, Oxford, UK

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William D Fraser Norwich Medical School, Faculty of Medicine and Health Sciences, University of East Anglia, Norwich, UK

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Tertius Hough MRC Mammalian Genetics Unit, MRC Harwell Institute, Harwell Science and Innovation Campus, Oxfordshire, UK

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Michael P Whyte Washington University in St Louis School of Medicine, Center for Metabolic Bone Disease and Molecular Research, St Louis, Missouri, USA

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Robin Lovell-Badge The Francis Crick Institute, London, 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, Churchill Hospital, Oxford, UK

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mechanisms that could result in such alterations in SOX3 expression ( Fig. 1B ). Firstly, deletions of X chromosome sequences may result in loss of a repressor or enhancer of SOX3 expression. Secondly, insertions of chromosome 2 sequences may result in

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-19-0478
Volume/Issue:
Volume 9: Issue 2
Open access
Danielle Christine Maria van der Kaay Erasmus University Medical Center, Department of Pediatrics, Subdivision of Endocrinology, Rotterdam, Netherlands

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Anne Rochtus Department of Pediatric Endocrinology, University Hospitals Leuven, Leuven, Belgium

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Gerhard Binder University Children’s Hospital, Pediatric Endocrinology, University of Tübingen, Tübingen, Germany

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Ingo Kurth Institute of Human Genetics, Medical Faculty, RWTH Aachen University, Aachen, Germany

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Dirk Prawitt Center for Paediatrics and Adolescent Medicine, University Medical Center, Mainz, Germany

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Irène Netchine Sorbonne Université, Centre de Recherche Saint-Antoine, INSERM, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France

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Gudmundur Johannsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology at Sahlgrenska University Hospital, Gothenburg, Sweden

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Anita C S Hokken-Koelega Erasmus University Medical Center, Department of Pediatrics, Subdivision of Endocrinology, Rotterdam, Netherlands

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Miriam Elbracht Institute of Human Genetics, Medical Faculty, RWTH Aachen University, Aachen, Germany

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Thomas Eggermann Institute of Human Genetics, Medical Faculty, RWTH Aachen University, Aachen, Germany

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-syndromic disorders, specific molecular alterations addressed by single locus or methylation tests as well as chromosomal disturbances are not expected; therefore, a panel of genes involved in isolated growth might be suitable to be screened. 1 Gene panel: targeted

Article Type:
Review Article
Collections:
Paediatric Endocrinology
DOI:
https://doi.org/10.1530/EC-22-0277
Volume/Issue:
Volume 11: Issue 11
Open access
Felix Reschke Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Torben Biester Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Thekla von dem Berge Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Dagmar Jamiolkowski Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Laura Hasse Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Francesca Dassie Padua University Hospital, Clinica Medica 3, Department of Medicine (DIMED), Padova, Veneto, Italy

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Pietro Maffei Padua University Hospital, Clinica Medica 3, Department of Medicine (DIMED), Padova, Veneto, Italy

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Katharina Klee Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Olga Kordonouri Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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Hagen Ott Auf Der Bult Children’s Hospital, Department of Paediatric Dermatology, Hannover, Germany

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Thomas Danne Auf Der Bult Children’s Hospital, Centre for Paediatric Endocrinology, Diabetology, and Clinical Research, Hannover, Germany

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alteration of the antigenic properties of the basement membrane. Many cell types in the skin express DPP-4, including keratinocytes, epithelial cells and T cells. DPP-4 is a cell surface plasminogen receptor that activates plasminogen and leads to the

Article Type:
Review Article
Collections:
Metabolic Syndrome and Diabetes
DOI:
https://doi.org/10.1530/EC-22-0410
Volume/Issue:
Volume 12: Issue 7
Open access
Dario de Biase Department of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) – Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy

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Federica Torricelli Laboratory of Translational Research, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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Moira Ragazzi Pathology Unit, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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Benedetta Donati Laboratory of Translational Research, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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Elisabetta Kuhn Pathology Unit, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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Michela Visani Department of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) – Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy

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Giorgia Acquaviva Department of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) – Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy

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Annalisa Pession Department of Pharmacy and Biotechnology (Dipartimento di Farmacia e Biotecnologie) – Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna, Bologna, Italy

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Giovanni Tallini Department of Medicine (Dipartimento di Medicina Specialistica, Diagnostica e Sperimentale) – Molecular Diagnostic Unit, Azienda USL di Bologna, University of Bologna School of Medicine, Bologna, Italy

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Simonetta Piana Pathology Unit, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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Alessia Ciarrocchi Laboratory of Translational Research, Azienda Unità Sanitaria Locale AUSL-IRCCS, Reggio Emilia, Italy

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mutation density (0.41 non-synonymous mutations per Mb, on average), ATCs are characterized by a high degree of genomic abnormalities that underscore their virulence and elevated mortality rate. Still few information on the genetic alterations associated

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0386
Volume/Issue:
Volume 7: Issue 12
Open access
Elham Barazeghi Department of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden

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Per Hellman Department of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden

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Gunnar Westin Department of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden

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Peter Stålberg Department of Surgical Sciences, Uppsala University, Uppsala University Hospital, Rudbeck Laboratory, Uppsala, Sweden

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give rise to carcinoid syndrome as a major cause of morbidity and mortality in approximately 20% of SI-NET patients. To date, genetic and epigenetic alterations in SI-NETs are poorly studied. Massive DNA sequencing analysis on SI-NETs revealed that

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-19-0279
Volume/Issue:
Volume 8: Issue 8
Open access
Ying Xu Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Lei Li Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Jihong Zheng Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Meng Wang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Bopei Jiang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Yue Zhai Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Liumei Lu Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Cong Zhang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Zhe Kuang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Xiaomei Yang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Li-Na Jin Department of Hematology, Changzheng Hospital, Naval Medical University, Shanghai, China

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Gufa Lin Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China
Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Orthopaedic Department of Tongji Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China

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Chao Zhang Translational Medical Center for Stem Cell Therapy and Institute for Regenerative Medicine, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China

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were retained in Xenopuslaevis ( 20 , 21 ). This allotetraploid Xenopus lineage evolves from two different diploid ancestors related to two current subgenomes, L (long chromosomes) and S (short chromosomes), by hybridization and allotetraploidization

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0179
Volume/Issue:
Volume 10: Issue 11
Open access
Klaus W Fagerstedt Department of Pathology, University of Helsinki, Helsinki, Finland

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Tom Böhling Department of Pathology, University of Helsinki, Helsinki, Finland
HUH Diagnostic Center and Helsinki University Hospital, Helsinki, Finland

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Harri Sihto Department of Pathology, University of Helsinki, Helsinki, Finland

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Tarja Salonen HUH Diagnostic Center and Helsinki University Hospital, Helsinki, Finland

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Fang Zhao Department of Pathology, University of Helsinki, Helsinki, Finland

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Mia Kero Department of Pathology, University of Helsinki, Helsinki, Finland
HUH Diagnostic Center and Helsinki University Hospital, Helsinki, Finland

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Leif C Andersson Department of Pathology, University of Helsinki, Helsinki, Finland

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Johanna Arola Department of Pathology, University of Helsinki, Helsinki, Finland
HUH Diagnostic Center and Helsinki University Hospital, Helsinki, Finland

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main deletions were 16q and 17p whole arms and almost the entire chromosome 19. Figure 1 H&E staining of the primary tumor and the metastasis. The neuroendocrine carcinoma (NEC) component of the primary tumor (A) ×10, (B) ×20. Some necrosis is

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-21-0206
Volume/Issue:
Volume 10: Issue 9
Open access