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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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). Cluster 2 has signature activation of MAP kinase signaling pathways. The following genes stand out: NF1, RET, HRAS, and TMEM127 (9–11). Cluster 3 (identified by The Cancer Genome Atlas) has WnT pathways based on a transcriptional signature, which

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-22-0091
Volume/Issue:
Volume 3: Issue 1
Open access
Katherine A English OCDEM, Radcliffe Department of Medicine, University of Oxford, Churchill Hospital, Oxford, UK

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Rajesh V Thakker OCDEM, Radcliffe Department of Medicine, University of Oxford, Churchill Hospital, Oxford, UK
Oxford NIHR Biomedical Research Centre, Oxford University Hospitals Trust, Oxford, UK

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Kate E Lines OCDEM, Radcliffe Department of Medicine, University of Oxford, Churchill Hospital, Oxford, UK
Oxford NIHR Biomedical Research Centre, Oxford University Hospitals Trust, Oxford, UK

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–Lindau tumour-suppressor ( VHL ), TSC complex ( TSC ) , neurofibromin 1( NF1 ), MutY DNA glycosylase, BRCA2 DNA repair-associated, cyclin-dependent kinase inhibitor 1B ( CDKN1B ), and checkpoint kinase 2 genes ( Crona & Skogseid 2016 , Scarpa et al. 2017

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EO-23-0003
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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% NF1 Autosomal dominant 7.7–14% +++ + + ++ ~12% SDHB Autosomal dominant 22–26% by age 60 ++ ++ +++ ++ 25–50% SDHD Autosomal dominant – paternal inheritance 43% by age 60 ++ +++ ++ +++ 3

Article Type:
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DOI:
https://doi.org/10.1530/EO-22-0044
Volume/Issue:
Volume 2: Issue 1
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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
Nele F Lenders Department of Endocrinology, St Vincent’s Hospital, Sydney, NSW, Australia
Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia

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Peter E Earls Department of Anatomical Pathology and Cytopathology, St Vincent’s Pathology, Sydney, NSW, Australia

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Warrick J Inder Department of Diabetes and Endocrinology, Princess Alexandra Hospital, Brisbane, QLD, Australia
Faculty of Medicine, the University of Queensland, Brisbane, QLD, Australia

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Ann I McCormack Department of Endocrinology, St Vincent’s Hospital, Sydney, NSW, Australia
Garvan Institute of Medical Research, Sydney, NSW, Australia
St Vincent’s Clinical School, University of New South Wales, Sydney, NSW, Australia

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a prevalence of approximately 1 in 1000 people, presenting with hormonal hyper or hypofunction, and/or mass effect symptoms ( Daly et al. 2006 , Fernandez et al. 2010 ). In addition, 10–15% of tumours demonstrate ‘aggressive behaviour

Article Type:
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DOI:
https://doi.org/10.1530/EO-22-0079
Volume/Issue:
Volume 3: Issue 1
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Damien A Leach Division of Cancer, Imperial Centre for Translational & Experimental Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK

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Rayzel C Fernandes Division of Cancer, Imperial Centre for Translational & Experimental Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK

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Charlotte L Bevan Division of Cancer, Imperial Centre for Translational & Experimental Medicine, Imperial College London, Hammersmith Hospital Campus, London, UK

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embedded in a surrounding stromal compartment comprised of smooth muscle cells, fibroblasts, vasculature, and immune cells ( Fig. 1A ). Cancer develops from the epithelial compartment ( Fig. 1A ), where it can be preceded by an inflammatory state, prostate

Article Type:
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DOI:
https://doi.org/10.1530/EO-22-0065
Volume/Issue:
Volume 2: Issue 1
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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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been identified associated with germline mutations in the mismatch repair genes MSH6 and MSH2 that cause Lynch syndrome ( Raymond et al. 2013 , Zheng et al. 2016 , Casey et al. 2018 ). Additionally, a small subset of adult ACC cases (1

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EO-21-0011
Volume/Issue:
Volume 1: Issue 1
Open access
Prabesh Khatiwada Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA
Center for Translational Immunology, Columbia University, New York, New York, USA

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Ujjwal Rimal Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA

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Zhengyang Han Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA
Dana-Farber Cancer Institute, Harvard University, Boston, Massachusetts, USA

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Lirim Shemshedini Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA

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a reversible covalent process that results in the attachment of ubiquitin to specific substrates by the sequential action of enzymes E1, E2, and E3 ( Schlesinger et al. 1975 ). Ubiquitin molecules are commonly added to specific lysine residues in

Article Type:
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DOI:
https://doi.org/10.1530/EO-23-0017
Volume/Issue:
Volume 4: Issue 1
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Trinidad Raices Laboratory of Molecular Endocrinology and Signal Transduction, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina
Centro de Investigaciones Endocrinológicas ’Dr. César Bergadá’ (CEDIE-CONICET-FEI), División de Endocrinología, Hospital de Niños Ricardo Gutiérrez, Buenos Aires, Argentina

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María Luisa Varela Departments of Neurosurgery, and Cell and Developmental Biology, University of Michigan, School of Medicine, Ann Arbor, Michigan, USA

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Adriana María Belén Abiuso Laboratory of Molecular Endocrinology and Signal Transduction, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina

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Elba N Pereyra Laboratory of Molecular Endocrinology and Signal Transduction, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina

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Carolina Mondillo Laboratory of Molecular Endocrinology and Signal Transduction, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina

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Omar P Pignataro Laboratory of Molecular Endocrinology and Signal Transduction, Instituto de Biología y Medicina Experimental (IBYME-CONICET), Buenos Aires, Argentina

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María Fernanda Riera Centro de Investigaciones Endocrinológicas ’Dr. César Bergadá’ (CEDIE-CONICET-FEI), División de Endocrinología, Hospital de Niños Ricardo Gutiérrez, Buenos Aires, Argentina

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Snyder JP Shoji M Pattnaik S Alam A El-Rayes BF 2016 Inhibition of NF-κB translocation by curcumin analogs induces G0/G1 arrest and downregulates thymidylate synthase in colorectal cancer . Cancer Letters 373 227 – 233 . ( https://doi.org/10

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DOI:
https://doi.org/10.1530/EO-22-0075
Volume/Issue:
Volume 3: Issue 1
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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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, germline BRCA1 mutation, and depression: a case report . Journal of Medical Case Reports 12 360. ( https://doi.org/10.1186/s13256-018-1890-x ) Bi WL Greenwald NF Ramkissoon SH Abedalthagafi M Coy SM Ligon KL Mei Y MacConaill L Ducar M

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https://doi.org/10.1530/EO-21-0033
Volume/Issue:
Volume 2: Issue 1
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