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Marie Plourde Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Caroline Manhes Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Gilles Leblanc Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Francine Durocher Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Martine Dumont Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Olga Sinilnikova Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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INHERIT BRCAs
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Jacques Simard Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada
Cancer Genomics Laboratory, Plate-Forme Mixte de Génétique Constitutionnelle des Cancers Fréquents, Canada Research Chair in Oncogenetics, Oncology and Molecular Endocrinology Research Center, Centre Hospitalier Universitaire de Québec and Laval University, Quebec G1V 4G2, Canada

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Introduction Most of the familial aggregation in breast cancer results predominantly from inherited susceptibility ( Lichtenstein et al . 2000 , Peto & Mack 2000 ). Germline mutations in high-penetrance cancer susceptibility genes such as breast

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JME-07-0101
Volume/Issue:
Volume 40: Issue 4
Free access
Ankita Agrawal Department of Human Metabolism, The Mellanby Centre for Bone Research, The University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK

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Alison Gartland Department of Human Metabolism, The Mellanby Centre for Bone Research, The University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK

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people at a greater risk of developing diseases and bone disorders. P2X7R and bone cancer Bone tissue provides a fertile setting for cancer cells and is a common metastatic site owing to this microenvironment. Signalling mechanisms involving purines and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-14-0226
Volume/Issue:
Volume 54: Issue 2
Free access
F M Fioretti Androgen Signalling Laboratory, Molecular Oncology, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK

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A Sita-Lumsden Androgen Signalling Laboratory, Molecular Oncology, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK

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C L Bevan Androgen Signalling Laboratory, Molecular Oncology, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK

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G N Brooke Androgen Signalling Laboratory, Molecular Oncology, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK
Androgen Signalling Laboratory, Molecular Oncology, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK

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Breast cancer Breast cancers (BCs) account for one in three newly diagnosed cases of cancer in women and led to 11 600 deaths in 2010 in the UK alone ( CRUK 2014 ). Incidence rates increased by 90% between 1971 and 2010, with the largest increase in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-14-0030
Volume/Issue:
Volume 52: Issue 3
Free access
Irene I Lee Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts, USA

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Nane C Kuznik Karlsruhe Institute of Technology, Institute of Toxicology and Genetics, Eggenstein-Leopoldshafen, Germany

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Jaice T Rottenberg Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts, USA

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Myles Brown Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, USA
Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts, USA

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Andrew C B Cato Karlsruhe Institute of Technology, Institute of Toxicology and Genetics, Eggenstein-Leopoldshafen, Germany

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experimentally tested. BAG1L and prostate cancer The regulation of AR activity by BAG1L and the driver role of the AR in prostate cancer progression has generated an interest in the action of BAG1L in prostate cancer. A link between BAG1L and prostate

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-19-0034
Volume/Issue:
Volume 62: Issue 4
Free access
Cathrin Brisken ISREC - Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Station 19, Lausanne, Switzerland
Breast Cancer Now Research Centre, Institute of Cancer Research, London, UK

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Valentina Scabia ISREC - Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Station 19, Lausanne, Switzerland

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Introduction A woman’s risk to get breast cancer is affected by her reproductive history and hence exposure to reproductive hormones. An early full-term pregnancy has protective effects ( MacMahon et al. , 1970 ), whereas risk increases with

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-20-0091
Volume/Issue:
Volume 65: Issue 1
Free access
Dagmara Rusinek Department of Nuclear Medicine and Endocrine Oncology, Maria Sklodowska‐Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Wybrzeze Armii Krajowej 15, 44-101 Gliwice, Poland

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Sylwia Szpak-Ulczok Department of Nuclear Medicine and Endocrine Oncology, Maria Sklodowska‐Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Wybrzeze Armii Krajowej 15, 44-101 Gliwice, Poland

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Barbara Jarzab Department of Nuclear Medicine and Endocrine Oncology, Maria Sklodowska‐Curie Memorial Cancer Center and Institute of Oncology, Gliwice Branch, Wybrzeze Armii Krajowej 15, 44-101 Gliwice, Poland

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Introduction Gene expression profiling of thyroid tumors has expanded our knowledge of the molecular biology of thyroid cancer. Several recent reviews addressed the biological and diagnostic aspects of microarray-based studies of thyroid cancer

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-11-0023
Volume/Issue:
Volume 47: Issue 3
Free access
Ali Salajegheh Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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Haleh Vosgha Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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Atiqur Md Rahman Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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Moein Amin Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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Robert Anthony Smith Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia
Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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Alfred King-Yin Lam Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia
Cancer Molecular Pathology, Faculty of Health, Pathology Queensland and Gold Coast University Hospital, School of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, Australia

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-205 can repress cancer proliferation, clonogenic survival, growth and aggressiveness by direct targeting of related genes such as E2F1 and BCl2 ( Vosgha et al . 2014 ). Nonetheless, the role of this miRNA has not been investigated in the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JME-15-0182
Volume/Issue:
Volume 55: Issue 3
Free access
James F H Pittaway Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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Leonardo Guasti Centre for Endocrinology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

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expression maintains an undifferentiated phenotype and promotes clonogenicity, findings suggestive of cancer stem cell-like functionality ( Kim et al. 2009 ). In the rat adrenal cortex, Dlk1 is co-expressed with Shh cells in the ZU ( Guasti et al. 2013

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-18-0122
Volume/Issue:
Volume 62: Issue 2
Free access
Amy R Dwyer Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA

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Thu H Truong Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA

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Julie H Ostrander Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA
Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, Minnesota, USA

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Carol A Lange Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA
Department of Medicine, Division of Hematology, Oncology, and Transplantation, University of Minnesota, Minneapolis, Minnesota, USA
Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota, USA

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cancer subtypes. However, increasing studies have implicated differential PR isoform expression in the etiology of breast cancer ( Mote et al. 2002 , 2015 , Rojas et al. 2017 , Lamb et al. 2018 ). Furthermore, PRs dramatically influence ER

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-19-0274
Volume/Issue:
Volume 65: Issue 1
Free access
Adrien Georges CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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Aurelie Auguste CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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Laurianne Bessière CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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Anne Vanet CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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Anne-Laure Todeschini CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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Reiner A Veitia CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France
CNRS UMR 7592, Université Paris Diderot, Institut Jacques Monod, 15 Rue Hélène Brion, 75013 Paris, France

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role in late folliculogenesis. For example, FOXL2 overexpression in GCT-derived cells causes induction of prostaglandin synthase (or COX2), but it has also been showed that it could repress the induction of this gene by ESR1 in breast cancer or

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JME-13-0159
Volume/Issue:
Volume 52: Issue 1
Free access