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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
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Yuanliang Li Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Yiying Guo Department of Integrative Oncology, China-Japan Friendship Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China

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Zixuan Cheng Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Chao Tian Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Yingying Chen Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Ruao Chen Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Fuhuan Yu Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China

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Yanfen Shi Department of Pathology, China-Japan Friendship Hospital, Beijing, China

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Fei Su Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing, China

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Shuhua Zhao Department of Biological Information Research, HaploX Biotechnology Co., Ltd, Shenzhen, Guangdong, China

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Zhizheng Wang Academic Department, HaploX Biotechnology, Co., Ltd, Shenzhen, Guangdong, China

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Jie Luo Department of Pathology, China-Japan Friendship Hospital, Beijing, China

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Huangying Tan Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing University of Chinese Medicine, Beijing, China
Department of Integrative Oncology, China-Japan Friendship Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
Department of Integrative Oncology, China-Japan Friendship Hospital, Beijing, China

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number deletion. The darker the color, the higher the frequency. A full-colour version of this figure can be found at https://doi.org/10.1530/ERC-22-0257 . Genetic alterations and survival To explore the potential correlation of gene

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-22-0257
Volume/Issue:
Volume 30: Issue 9
Open 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
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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decades to improve the knowledge of molecular pathogenesis of DTC. This led to the identification of a set of molecular alterations with demonstrated/putative pathogenetic role ( Xing 2013 ). These abnormalities are heterogeneous, including both genetic

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-16-0372
Volume/Issue:
Volume 23: Issue 11
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
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Mouna Tabebi Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden

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Peter Söderkvist Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden
Clinical Genomics Linköping, Linköping University, Linköping, Sweden

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Oliver Gimm Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden
Department of Surgery, Linköping University, Linköping, Sweden

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of limited value. New treatment options are therefore sought after. Nowadays, the genetic background of most PPGLs is well known. They are one of the most heritable tumors, where germline and somatic genetic alterations in non

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-22-0217
Volume/Issue:
Volume 30: Issue 1
Free access
Fidéline Bonnet-Serrano Institut Cochin, INSERM U1016, CNRS UMR8104, Paris Descartes University, Paris, France
Hormonal Biology Laboratory, Assistance Publique Hôpitaux de Paris, Hôpital Cochin, Paris, France

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Jérôme Bertherat Institut Cochin, INSERM U1016, CNRS UMR8104, Paris Descartes University, Paris, France
Department of Endocrinology, Assistance Publique Hôpitaux de Paris, Hôpital Cochin, Paris, France

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. Phosphodiesterases (PDE), involved in cAMP degradation, act as negative regulators of this pathway. (B) cAMP/PKA signaling pathway genetic alterations in PPNAD 1: PRKAR1A inactivation (germline mutation + somatic second-hit); 2: phosphodiesterases ( PDE11A or PD8

Article Type:
Review Article
DOI:
https://doi.org/10.1530/ERC-17-0361
Volume/Issue:
Volume 25: Issue 3
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
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
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Darren Cowzer Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Ronak H Shah Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Joanne F Chou Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Ritika Kundra Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Sippy Punn Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Laura Fiedler Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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April DeMore Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Marinela Capanu Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Michael F Berger Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Department of Pathology and laboratory medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA

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Diane Reidy-Lagunes Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill Medical College of Cornell University, New York, New York, USA

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Nitya Raj Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA
Weill Medical College of Cornell University, New York, New York, USA

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-differentiated panNENs more frequently harbor alterations in the tumor suppressor gene MEN1 , the chromatin remodeling genes ( DAXX / ATRX ), and in the mTOR pathway ( Jiao et al. 2011 ). In contrast, genetic profiling of poorly differentiated neuroendocrine

Article Type:
Research Article
DOI:
https://doi.org/10.1530/ERC-23-0292
Volume/Issue:
Volume 31: Issue 4
Restricted access