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José V Lima Jr Department of Medicine, Division of Endocrinology and Metabolism, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil
Santa Casa de São Paulo School of Medical Sciences, São Paulo, SP, Brazil
Fleury Group, São Paulo, SP, Brazil

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Nilza M Scalissi Santa Casa de São Paulo School of Medical Sciences, São Paulo, SP, Brazil

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Kelly C de Oliveira Department of Medicine, Division of Endocrinology and Metabolism, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil

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Susan C Lindsey Department of Medicine, Division of Endocrinology and Metabolism, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil

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Caroline Olivati Fleury Group, São Paulo, SP, Brazil

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Elisa Napolitano Ferreira Fleury Group, São Paulo, SP, Brazil

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Claudio E Kater Department of Medicine, Division of Endocrinology and Metabolism, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP, Brazil

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deposited in PubMed, Arup, ClinVar, and Varsome). The 23 genes analyzed were ATM, ATR, CDKN2A, EGLN1, FH, HRAS, KIF1B, KMT2D, MAX, MDH2, MERTK, MET, NF1, PIK3CA, RET, SDHA, SDHAF2, SDHB, SDHC, SDHD, TMEM127, TP53, and VHL. The genetic analysis of 47

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-22-0091
Volume/Issue:
Volume 3: Issue 1
Open access
Christie G Turin Department of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Colorado, Aurora, Colorado, USA

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Molly M Crenshaw Department of Pediatrics, Combined Pediatrics-Medical Genetics Residency Program, University of Colorado, Aurora, Colorado, USA

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Lauren Fishbein Department of Medicine, Division of Endocrinology, Metabolism and Diabetes, University of Colorado, Aurora, Colorado, USA
Division of Biomedical Informatics and Personalized Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA

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skull base to pelvis every 2 years. MAX- associated PCC/PGL Pheochromocytoma, paraganglioma At diagnosis: Plasma-free metanephrines or 24-h urine-fractionated metanephrines and full-body MRI from skull base to pelvis. Annual biochemical

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EO-22-0044
Volume/Issue:
Volume 2: Issue 1
Open access
Catherine M Skefos The University of Texas MD Anderson Cancer Center, Clinical Cancer Genetics Program, Houston, Texas, USA

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Pamela L Brock The Ohio State University College of Medicine, Division of Human Genetics, Comprehensive Cancer Center, Columbus, Ohio, USA

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Erica Blouch Massachusetts General Hospital Cancer Center, Boston, Massachusetts, USA

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Samantha E Greenberg Department of Health Care Sciences, UT Southwestern Medical Center, Dallas, Texas, USA

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). This hereditary predisposition falls under the spectrum of hereditary paraganglioma–pheochromocytoma (PPGL) syndromes. Additional genes that cause hereditary PPGL include the other SDHx genes ( SDHB , SDHC , SDHD , and SDHAF2 ), MAX , and TMEM127

Article Type:
Commentary
DOI:
https://doi.org/10.1530/EO-23-0043
Volume/Issue:
Volume 4: Issue 1
Open access
Nada Younes Division of Endocrinology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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Isabelle Bourdeau Division of Endocrinology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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Harold Olney Division of Hematology and Medical Oncology, Department of Medicine, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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Paul Perrotte Division of Urology, Department of Surgery, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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Odile Prosmanne Department of Radiology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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Mathieu Latour Department of Pathology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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David Roberge Division of Radiation Oncology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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André Lacroix Division of Endocrinology, and Research Center, Centre hospitalier de l’Université de Montréal (CHUM), Montréal, Québec, Canada

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, pancreas and anterior cortex of the left kidney. The mass was highly avid on FDG-PET (standardized uptake value, SUV max 22) with area of calcification and necrosis. No other hypermetabolic lesions or adenopathies were found. The consultant hematology

Article Type:
Case Report
DOI:
https://doi.org/10.1530/EO-21-0031
Volume/Issue:
Volume 1: Issue 1
Open access
Sofia Maria Lider Burciulescu CI Parhon National Institute of Endocrinology, Bucharest, Romania

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Caren Randon Department of Thoracic and Vascular Surgery, Ghent University Hospital & Department of Human Structure and Repair, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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Frederic Duprez Department of Radiotherapy-Oncology, Ghent University Hospital, Ghent Belgium & Department of Human Structure and Repair, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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Wouter Huvenne Department of Head and Neck Surgery, Ghent University Hospital & Department of Head & Skin, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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David Creytens Department of Pathology, Ghent University Hospital, Ghent University & Department of Diagnostic Sciences, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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Kathleen B M Claes Center for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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Robin de Putter Center for Medical Genetics, Ghent University Hospital & Department of Biomolecular Medicine, Faculty of Medicine and Health Sciences, UGent, Ghent, Belgium

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Guy T’Sjoen Department of Endocrinology, Ghent University Hospital & Department of Internal Medicine & Pediatrics, Faculty of Medicine and Health Sciences, UGent , Ghent, Belgium

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Corin Badiu CI Parhon National Institute of Endocrinology, Bucharest, Romania
Carol Davila University of Medicine and Pharmacy, Bucharest, Romania

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Bruno Lapauw Department of Endocrinology, Ghent University Hospital & Department of Internal Medicine & Pediatrics, Faculty of Medicine and Health Sciences, UGent , Ghent, Belgium

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included the most frequently mutated genes in PPGL: RET, VHL, NF1, MAX, SDHA, SDHB, SDHC, SDHD, SDHAF2, and TMEM127 . Depending on phenotypic features and/or year of diagnosis, patients were tested for a variable number of these genes. For patients with

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-22-0040
Volume/Issue:
Volume 3: Issue 1
Open access
Mark S Stein Knox Private Hospital, Wantirna, Victoria, Australia

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Victor Kalff Molecular Imaging and Therapeutic Nuclear Medicine, Cancer Imaging, Prostate Cancer Theranostics and Imaging Centre of Excellence (ProsTIC), Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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Scott G Williams Radiation Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Sir Peter MacCallum Department of Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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Declan G Murphy Sir Peter MacCallum Department of Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Division of Cancer Surgery, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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Peter G Colman Department of Diabetes and Endocrinology, The Royal Melbourne Hospital and University of Melbourne Department of Medicine, Parkville, Victoria, Australia

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Michael S Hofman Molecular Imaging and Therapeutic Nuclear Medicine, Cancer Imaging, Prostate Cancer Theranostics and Imaging Centre of Excellence (ProsTIC), Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia
Sir Peter MacCallum Department of Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia

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osseous. Given the limited number of exendin-avid lesions, the proportion of total administered dose expressed by these avid lesions was not calculated. However, the SUV max of these lesions was 4.3 (left proximal humerus), 1.5 (left posterior 8th rib

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-23-0015
Volume/Issue:
Volume 4: Issue 1
Open access
Sylvia L Asa Department of Pathology, University Hospitals Cleveland Medical Center, Case Western Reserve University, Cleveland, Ohio, USA

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Shereen Ezzat Department of Medicine, University Health Network, University of Toronto, Toronto, Ontario, Canada

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associated with other NETs. These include multiple endocrine neoplasia types 1, 4 and 5 due to mutations in MEN1, CDKN1B and MAX , respectively, all of which are implicated in the development of NETs in other organs ( Ezzat et al. 2018 , Asa et al

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EO-22-0041
Volume/Issue:
Volume 2: Issue 1
Open access
Eleanor Fewings Academic Department of Medical Genetics, National Institute for Health Research Cambridge Biomedical Research Centre, University of Cambridge, Cambridge, UK

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Serena Khoo Sert Kim Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Alexey Larionov Academic Department of Medical Genetics, National Institute for Health Research Cambridge Biomedical Research Centre, University of Cambridge, Cambridge, UK

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Alison Marker Department of Histopathology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Olivier Giger Department of Pathology, University of Cambridge, Cambridge, UK

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Ashley Shaw Department of Radiology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Graeme R Clark Academic Department of Medical Genetics, National Institute for Health Research Cambridge Biomedical Research Centre, University of Cambridge, Cambridge, UK

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Vasilis Kosmoliaptsis Department of Surgery, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Benjamin G Challis Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Marc Tischkowitz Academic Department of Medical Genetics, National Institute for Health Research Cambridge Biomedical Research Centre, University of Cambridge, Cambridge, UK
East Anglian Medical Genetics Service, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Ruth T Casey Academic Department of Medical Genetics, National Institute for Health Research Cambridge Biomedical Research Centre, University of Cambridge, Cambridge, UK
Department of Endocrinology, Cambridge University Hospital NHS Foundation Trust, Cambridge, UK

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Cortisol Cortisol Site Left Left Right Right Left Right Left Right Left Left Max diameter (mm) 105 205 130 105 135 78 38 170 68 20 Imaging characterization N/A N/A N/A Indeterminate

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-21-0011
Volume/Issue:
Volume 1: Issue 1
Open access
Sandra Pekic School of Medicine, University of Belgrade, Belgrade, Serbia
Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center Belgrade, Belgrade, Serbia

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Marko Stojanovic School of Medicine, University of Belgrade, Belgrade, Serbia
Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Center Belgrade, Belgrade, Serbia

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Vera Popovic School of Medicine, University of Belgrade, Belgrade, Serbia

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1 and 4, familial isolated pituitary adenomas, succinate dehydrogenase mutations ( SDHA , SDHB , SDHC , SDHD , MAX , TMEM 127 ) and other conditions (Mc Cune Albright Sy, Carney complex, neurofibromatosis type 1, von Hippel–Lindau syndrome and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EO-21-0033
Volume/Issue:
Volume 2: Issue 1
Open access