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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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possible new treatment strategies. For this purpose, we applied massive parallel sequencing (NGS) with subsequent assessments of genetic alterations, in a large biobank of HG GEP-NEN samples. Patients and samples The samples were from patients

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
L C J Dorssers
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T van Agthoven
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A Brinkman
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ABSTRACT

Genetic changes in breast tumour cells may contribute to the development of resistance during antiestrogen therapy. The results of our experiments in support of this hypothesis and the identification of the first genetic locus involved in development of tamoxifen resistance in vitro are reviewed.

Endocrine-Related Cancer (1995) 2 123-126

Article Type:
Research Article
DOI:
https://doi.org/10.1677/erc.0.0201123
Volume/Issue:
Volume 2: Issue 1
Restricted access
M Xing Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, 1830 E. Monument St/Suite 333 Baltimore, MD 21287, USA

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alterations, some of which are seen only in this cancer. The classical oncogenic genetic alterations commonly seen in thyroid cancer include Ras mutations ( Fagin 2002 , Bongarzone & Pierotti 2003 ), RET/PTC rearrangements ( Nikiforov 2002 , Santoro et

Article Type:
Review Article
DOI:
https://doi.org/10.1677/erc.1.0978
Volume/Issue:
Volume 12: Issue 2
Free access
Valdemar Máximo i3S Instituto de Investigação e Inovação em Saúde, Porto, Portugal
Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal
Department of Pathology and Oncology, Medical Faculty, University of Porto, Porto, Portugal

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Miguel Melo i3S Instituto de Investigação e Inovação em Saúde, Porto, Portugal
Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal
Department of Endocrinology, Diabetes and Metabolism, Centro Hospitalar e Universitário de Coimbra, Medical Faculty, University of Coimbra, Coimbra, Portugal

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Yingjie Zhu Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, USA

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Andrea Gazzo Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, USA

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Manuel Sobrinho Simões i3S Instituto de Investigação e Inovação em Saúde, Porto, Portugal
Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal
Department of Pathology and Oncology, Medical Faculty, University of Porto, Porto, Portugal
Department of Pathology, Hospital São João, Porto 4200-319, Portugal

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Arnaud Da Cruz Paula i3S Instituto de Investigação e Inovação em Saúde, Porto, Portugal
Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal

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Paula Soares i3S Instituto de Investigação e Inovação em Saúde, Porto, Portugal
Institute of Molecular Pathology and Immunology, University of Porto, Porto, Portugal
Department of Pathology and Oncology, Medical Faculty, University of Porto, Porto, Portugal

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. 2017 ). Previous pancancer genetic studies comparing primary and metastatic carcinomas across 50 cancer types have shown a significantly higher frequency of TERT promoter mutations and CDKN2A genetic alterations in metastases from PTCs than in

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-23-0144
Volume/Issue:
Volume 31: Issue 2
Restricted access
Vincenzo Marotta IOS & COLEMAN Srl, Naples, Italy

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Concetta Sciammarella IOS & COLEMAN Srl, Naples, Italy

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Annamaria Colao Department of Clinical Medicine and Surgery, Federico II University, Naples, Italy

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Antongiulio Faggiano Thyroid and Parathyroid Surgery Unit, Istituto Nazionale per lo Studio e la Cura dei Tumori-IRCCS “Fondazione G. Pascale”, Naples, Italy

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-called molecular prognostication into ‘real-life’ clinical practice is still yet to be performed. In this review, we will analyse the current knowledge about prognostic significance and the actual role of the most common and best studied genetic alterations related

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0372
Volume/Issue:
Volume 23: Issue 11
Free access
Carles Zafon Diabetes and Metabolism Research Unit (VHIR) and Department of Endocrinology, University Hospital Vall d’Hebron and Autonomous University of Barcelona, Barcelona, Spain
Consortium for the Study of Thyroid Cancer (CECaT), Catalonia, Spain

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Joan Gil Program of Predictive and Personalized Medicine of Cancer, Germans Trias i Pujol Research Institute (PMPPC-IGTP), Barcelona, Spain

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Beatriz Pérez-González Program of Predictive and Personalized Medicine of Cancer, Germans Trias i Pujol Research Institute (PMPPC-IGTP), Barcelona, Spain

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Mireia Jordà Consortium for the Study of Thyroid Cancer (CECaT), Catalonia, Spain
Program of Predictive and Personalized Medicine of Cancer, Germans Trias i Pujol Research Institute (PMPPC-IGTP), Barcelona, Spain

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/AKT pathway is involved in the progression of FTC. Recently, the genetic landscape of some thyroid cancer histotypes has been largely deciphered ( Cancer Genome Atlas Research Network 2014 , Kunstman et al. 2015 ), and some of these genetic alterations have

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-19-0093
Volume/Issue:
Volume 26: Issue 7
Free access
Yong Lin
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Xiaofei Jiang
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Ye Shen Department of Laboratory Medicine, Institute of Endocrinology and Diabetologia, Division of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Fudan University, 12 Central Urumqi Road, Shanghai 200040, People's Republic of China

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Min Li
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Huili Ma
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Mingzhao Xing Department of Laboratory Medicine, Institute of Endocrinology and Diabetologia, Division of Endocrinology and Metabolism, Huashan Hospital, Shanghai Medical College, Fudan University, 12 Central Urumqi Road, Shanghai 200040, People's Republic of China

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Yuan Lu
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2004 ). However, genetic alterations, which are the driving force for human tumorigenesis and pathogenesis, have in general been unknown in pituitary tumors. Given the frequent mutations and amplifications of the PIK3CA gene in many human tumors and

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-08-0167
Volume/Issue:
Volume 16: Issue 1
Free access
Cristina Romei Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Raffaele Ciampi Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Pinuccia Faviana Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Laura Agate Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Eleonora Molinaro Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Valeria Bottici Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Fulvio Basolo Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Paolo Miccoli Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Furio Pacini Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Aldo Pinchera Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy
Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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Rossella Elisei Departments of, Endocrinology and Metabolism, Oncology, Surgery, Department of Internal Medicine, AMBISEN Center, University of Pisa, 56100 Pisa, Italy

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associated with the more aggressive phenotype, no clear correlation between RET/PTC rearrangements and a better or worse prognosis has been documented ( Basolo et al . 2001 ). The V600E mutation is the only BRAF genetic alteration (BRAF V600E ) consistently

Article Type:
Research Article
DOI:
https://doi.org/10.1677/ERC-07-0130
Volume/Issue:
Volume 15: Issue 2
Free access
Alyaksandr V Nikitski Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Marina N Nikiforova Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Linwah Yip Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Esra Karslioglu-French Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Sally E Carty Division of Endocrine Surgery, Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Yuri E Nikiforov Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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( Cancer Genome Atlas Research 2014 , Yoo et al. 2016 ) and likely DNA copy number alterations (CNA) in HCC ( Ganly et al. 2018 , Gopal et al. 2018 ). In PDC and AC, such 'early' genetic alterations are found in combination with mutations in TERT

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-21-0095
Volume/Issue:
Volume 28: Issue 9
Restricted access
M Lacroix Laboratoire Jean-Claude Heuson de Cancérologie Mammaire, Institut Jules Bordet, Université Libre de Bruxelles, 127 boulevard de Waterloo, B-1000 Bruxelles, Brussels, Belgium

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R-A Toillon Laboratoire Jean-Claude Heuson de Cancérologie Mammaire, Institut Jules Bordet, Université Libre de Bruxelles, 127 boulevard de Waterloo, B-1000 Bruxelles, Brussels, Belgium

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G Leclercq Laboratoire Jean-Claude Heuson de Cancérologie Mammaire, Institut Jules Bordet, Université Libre de Bruxelles, 127 boulevard de Waterloo, B-1000 Bruxelles, Brussels, Belgium

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are expected to often be significantly different from those observed in BCCs in situ . In fact, a number of recent data—of pathological, molecular and genetic nature—have revealed that despite increasing genetic alteration, the ‘portrait’ of

Article Type:
Research Article
DOI:
https://doi.org/10.1677/erc.1.00758
Volume/Issue:
Volume 11: Issue 3
Free access