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Kathleen A Luckett Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Jennifer R Cracchiolo Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Gnana P Krishnamoorthy Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Luis Javier Leandro-Garcia Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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James Nagarajah Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Mahesh Saqcena Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Rona Lester Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Soo Y Im Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Zhen Zhao Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Scott W Lowe Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Elisa de Stanchina Antitumor Assessment Core Facility, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Eric J Sherman Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill-Cornell Medical College, New York, New York, USA

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Alan L Ho Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill-Cornell Medical College, New York, New York, USA

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Steven D Leach Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Jeffrey A Knauf Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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James A Fagin Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill-Cornell Medical College, New York, New York, USA

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that pSMAD2/3 binds to the thyroid lineage transcription factor PAX8 and impairs its transactivation of the sodium iodide symporter ( Nis ), and that this is reversed by expression of SMAD7 ( Costamagna et al. 2004 , Riesco-Eizaguirre et al. 2009

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-21-0017
Volume/Issue:
Volume 28: Issue 6
Open access
Catherine Zabkiewicz Cardiff China Medical Research Collaborative Cardiff University School of Medicine, Cardiff, UK

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Jeyna Resaul Cardiff China Medical Research Collaborative Cardiff University School of Medicine, Cardiff, UK

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Rachel Hargest Cardiff China Medical Research Collaborative Cardiff University School of Medicine, Cardiff, UK

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Wen Guo Jiang Cardiff China Medical Research Collaborative Cardiff University School of Medicine, Cardiff, UK

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Lin Ye Cardiff China Medical Research Collaborative Cardiff University School of Medicine, Cardiff, UK

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, Smad2, Map3k1, Tob1, Ywhag/14-3-3γ, Ywhab/14-3-3β, Smad5, Zfp36, Xbp1, Mapk12 and Snail ( Perdigao-Henriques et al . 2016 ). BMP-2 appears to promote motility and invasiveness of MCF-7 and MDA-MB-231 cells, both in vitro and in vivo ( Clement et

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-17-0139
Volume/Issue:
Volume 24: Issue 10
Open access
Bethany Smith Department of Medicine, Samuel Ochin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA

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Priyanka Agarwal Department of Medicine, Samuel Ochin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA

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Neil A Bhowmick Department of Medicine, Samuel Ochin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA
Greater Los Angeles Veterans Administration, Los Angeles, California, USA

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. 2011 ). It is possible that the specificity of a miR to a particular TGF-β ligand isoform or downstream effectors may limit some of these unwanted effects. Of these effectors, Smad2, Smad3 and Smad4 activate downstream transcription, but can be

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0525
Volume/Issue:
Volume 24: Issue 5
Open access
Xiaoli Liu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Chunhai Zhang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Xiaomiao Wang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Can Cui Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Hanwen Cui Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Baishu Zhu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Anqi Chen Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Lu Zhang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Jingwei Xin Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Qingfeng Fu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Gianlorenzo Dionigi Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
Division of Surgery, Istituto Auxologico Italiano, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy

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Hui Sun Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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, as described previously ( Zhang et al. 2017 b ). Antibodies against TGFBR2 (mouse mAb, Cat#: 66636-1-Ig, 1:2000), USP15 (Mouse mAb, Cat#: 67557-1-Ig, 1:5000) and phosphorylated SMAD3 (Rabbit mAb, Cat#: ab52903, 1:5000) were purchased from

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-22-0221
Volume/Issue:
Volume 30: Issue 3
Open access
Andreas Venizelos K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Hege Elvebakken Department of Oncology, Ålesund Hospital, Møre og Romsdal Hospital Trust, Ålesund, Norway
Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway

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Aurel Perren Institute of Pathology, University of Bern, Bern, Switzerland

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Oleksii Nikolaienko K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Wei Deng K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Inger Marie B Lothe Department of Pathology, Oslo University Hospital, Oslo, Norway

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Anne Couvelard Department of Pathology, Université de Paris, Bichat Hospital, AP-HP, Paris, France

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Geir Olav Hjortland Department of Oncology, Oslo University Hospital, Oslo, Norway

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Anna Sundlöv Departmentt of Oncology, Skåne University Hospital, Lund, Sweden
Department of Medical Radiation Physics, Lund University, Lund, Sweden

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Johanna Svensson Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Harrish Garresori Department of Oncology, Stavanger University Hospital, Stavanger, Norway

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Christian Kersten Department of Research, Hospital of Southern Norway, Kristiansand, Norway

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Eva Hofsli Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
Department of Oncology, St.Olavs Hospital, Trondheim, Norway

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Sönke Detlefsen Department of Pathology, Odense University Hospital, Odense, Denmark
Department of Clinical Medicine, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark

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Merete Krogh Department of Oncology, Odense University Hospital, Odense, Denmark

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Halfdan Sorbye Department of Oncology, Haukeland University Hospital, Bergen, Norway
Department of Clinical Science, University of Bergen, Bergen, Norway

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Stian Knappskog K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Table 1). A prediction model for the classification of tumours into the categories LC-NEC or NET G3 was built, based on mutational status of nine genes ( APC , ATRX , BRAF , DAXX , KRAS , MEN1 , MYO5B , SMAD2 and TP53 ). Classification was

Article Type:
Research Article
Collections:
Top-cited articles of 2023
DOI:
https://doi.org/10.1530/ERC-21-0152
Volume/Issue:
Volume 29: Issue 1
Open access
Maria Angela De Stefano Department of Public Health, University of Naples “Federico II”, Naples, Italy

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Tommaso Porcelli Department of Public Health, University of Naples “Federico II”, Naples, Italy

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Martin Schlumberger Department of Endocrine Oncology, Gustave Roussy and University Paris-Saclay, Villejuif, France

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Domenico Salvatore Department of Public Health, University of Naples “Federico II”, Naples, Italy
CEINGE Biotecnologie Avanzate Scarl, Naples, Italy

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demonstrated that mutated BRAF V600E increases the TGFB1 expression ( Riesco-Eizaguirre et al. 2009 , Knauf et al. 2011 ) and that in different cell contexts, TGF-β induces the transcription of human D3 through a Smad-dependent pathway ( Azouzi et

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-23-0015
Volume/Issue:
Volume 30: Issue 5
Open access
Mina Sattari Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Annika Kohvakka Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Elaheh Moradi A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland

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Hanna Rauhala Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Henna Urhonen Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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William B Isaacs The James Buchanan Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, Maryland, USA

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Matti Nykter Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Teemu J Murtola Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland
Department of Urology, Tampere University Hospital, Tampere, Finland

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Teuvo L J Tammela Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland
Department of Urology, Tampere University Hospital, Tampere, Finland

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Leena Latonen Foundation for the Finnish Cancer Institute, Helsinki, Finland
Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland

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G Steven Bova Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Juha Kesseli Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland

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Tapio Visakorpi Faculty of Medicine and Health Technology, Tampere University and Tays Cancer Center, Tampere University Hospital, Tampere, Finland
Fimlab Laboratories Ltd, Tampere University Hospital, Tampere, Finland

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, Wu et al. 2020 , Zhang et al. 2020 ). For example, multiple lncRNAs, such as PCA3, a well-known example of PCa-specific lncRNAs, have been found to be related to PCa ( Bussemakers et al. 1999 , De Kok et al. 2002 , Martens-Uzunova et al

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-22-0247
Volume/Issue:
Volume 30: Issue 8
Open access
Tobias Hofving Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Yvonne Arvidsson Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Bilal Almobarak Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Linda Inge Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Roswitha Pfragner Institute of Pathophysiology and Immunology, Center for Molecular Medicine, Medical University of Graz, Graz, Austria

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Marta Persson Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Göran Stenman Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Erik Kristiansson Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden

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Viktor Johanson Department of Surgery, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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Ola Nilsson Sahlgrenska Cancer Center, Department of Pathology and Genetics, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

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of parts or whole chromosome 18 is the most common genomic event in SINETs (found in 60‒70% of the tumours). The GOT1 cell line showed loss of a 1.8 Mb segment of 18q, including the tumour suppressor SMAD4 ( Fig. 3A ). The GOT1 cell line originated

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-17-0445
Volume/Issue:
Volume 25: Issue 3
Open access
Xuan Chen Department of Breast Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Sixuan Liu Department of Breast Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Xue Peng Department of Breast Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Xiangyun Zong Department of Breast Surgery, Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China

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receptor complex with AMHRI. This complex phosphorylates AMHRI and activates serine/threonine protein kinase. Subsequently, intracellular Smad-proteins (R-SMads1/5/8) detach from the receptor complexes, allowing several proteins to enter the nucleus to

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-23-0060
Volume/Issue:
Volume 30: Issue 10
Open access
Tsai-Der Chuang Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610-0294, USA

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Harekrushna Panda Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610-0294, USA

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Xiaoping Luo Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610-0294, USA

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Nasser Chegini Department of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610-0294, USA

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regulatory function of microRNAs (miRNAs) on protein-coding gene expression through interacting with their 3′ UTR resulting in their posttranscriptional repression ( Djuranovic et al . 2011 ). Through this mechanism, miRNAs regulate various aspects of normal

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-12-0007
Volume/Issue:
Volume 19: Issue 4
Open access
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