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Federica Morani Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Rossella Titone Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Loredana Pagano Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Alessandra Galetto Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Oscar Alabiso Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Gianluca Aimaretti Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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Ciro Isidoro Laboratory of Molecular Pathology, Unit of Oncology, Department of Health Sciences

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and oncosuppressor genes regulate the induction of autophagy. Autophagy is also epigenetically regulated through the methylation of autophagy regulatory genes, the activity of histone deacetylases (HDAC), and the expression of microRNAs (miRNAs). Here

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Alastair Davies Vancouver Prostate Centre, Vancouver, British Columbia, Canada
Department of Urologic Sciences, Faculty of Medicine, University of British Columbia, British Columbia, Canada

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Amina Zoubeidi Vancouver Prostate Centre, Vancouver, British Columbia, Canada
Department of Urologic Sciences, Faculty of Medicine, University of British Columbia, British Columbia, Canada

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Luke A Selth Flinders Centre for Innovation in Cancer, Flinders University, College of Medicine and Public Health, Bedford Park, South Australia, Australia
Dame Roma Mitchell Cancer Research Laboratories and Freemasons Foundation Centre for Men’s Health, Adelaide Medical School, The University of Adelaide, Adelaide, South Australia, Australia

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facilitate the activation of pluripotency networks mediated, in part, through de-repression of the pluripotency transcription factor SOX2 as well as the epigenetic modifier, enhancer of zeste-homolog 2 (EZH2) ( Choi et al . 2011 , Kareta et al . 2015 , Ku

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Sophie Moog PARCC, INSERM UMR970, Equipe Labellisée par la Ligue contre le Cancer, Paris, France
Université de Paris, Paris, France

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Charlotte Lussey-Lepoutre PARCC, INSERM UMR970, Equipe Labellisée par la Ligue contre le Cancer, Paris, France
Department of Nuclear Medicine, Sorbonne University, Pitie-Salpetriere Hospital, Paris, France

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Judith Favier PARCC, INSERM UMR970, Equipe Labellisée par la Ligue contre le Cancer, Paris, France
Université de Paris, Paris, France

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review provides an overview of the pathophysiology and then focuses on clinical implications of the epigenetic and metabolic reprogramming of SDH-deficient PPGL. Figure 1 Epigenetic and metabolic reprogramming of SDH-deficient pheochromocytomas and

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Sandra Rodríguez-Rodero Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain
Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Elías Delgado-Álvarez Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Agustín F Fernández Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Juan L Fernández-Morera Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Edelmiro Menéndez-Torre Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Mario F Fraga Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain
Endocrinology and Nutrition Service Hospital Universitario Central de Asturias, Av. Julian Clavería s/n, 33006 Oviedo, Spain

Cancer Epigenetics Laboratory Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Universidad de Oviedo, 33006 Oviedo, Spain

Department of Immunology and Oncology National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain

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Introduction Epigenetics is defined as the study of those stable genetic modifications that result in changes in function and gene expression without altering the DNA sequence. The term was first described in 1942 by C H Waddington as the study of

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Catia Mio Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Elisa Lavarone Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Ketty Conzatti Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Federica Baldan Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Barbara Toffoletto Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Cinzia Puppin Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Sebastiano Filetti Department of Internal Medicine and Medical Specialties, University ‘Sapienza’, Rome, Italy

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Cosimo Durante Department of Internal Medicine and Medical Specialties, University ‘Sapienza’, Rome, Italy

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Diego Russo Department of Health Sciences, University of Catanzaro ‘Magna Graecia’, Catanzaro, Italy

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Arturo Orlacchio Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York, USA

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Antonio Di Cristofano Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York, USA

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Carla Di Loreto Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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Giuseppe Damante Department of Medical and Biological Sciences, University of Udine, Udine, Italy

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, represent the least common but most lethal thyroid cancer subtype. Indeed, they are characterized by genetic and epigenetic aberrations that make them unresponsive to treatments based on radioiodine administration ( Arturi et al. 2000 , Schlumberger et

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Kevin C Knower Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia

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Sarah Q To Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia
Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia

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Yuet-Kin Leung Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia

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Shuk-Mei Ho Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia

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Colin D Clyne Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia
Cancer Drug Discovery, Department of Molecular Biology and Biochemistry, Department of Environmental Health, MIMR-PHI Institute of Medical Research, PO BOX 5152, Clayton, Victoria 3168, Australia

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diseases like cardiovascular, pulmonary or neurodegenerative disorders to name a few ( Irigaray et al . 2007 , Mathers et al . 2010 ). In such instances, early-life epigenetic programming and also those encountered during adult life are large

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A Karpathakis University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK
University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK

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H Dibra University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK

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C Thirlwell University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK
University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK

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Introduction Epigenetics can be defined as the study of heritable changes in gene expression without alteration of the underlying DNA sequence. In recent years, the understanding of epigenetic drivers of tumorigenesis has developed rapidly in

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S Fontanière
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J Tost
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A Wierinckx
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J Lachuer
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J Lu
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N Hussein
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F Busato
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I Gut
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Z-Q Wang
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C-X Zhang
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methylation. Our work highlights the early involvement of both genetic and epigenetic mechanisms in tumorigenesis of β-cells related to MEN1 inactivation. Materials and methods Men1 F/F -RipCre + pancreatic β

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William D Foulkes Program in Cancer Genetics, Departments of Oncology and Human Genetics, 546 Pine Avenue West, McGill University, Montreal, Quebec, Canada H2W 1S6

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the mechanisms of loss of heterozygosity in retinoblastoma was being published, another theme was being explored. Feinberg & Vogelstein (1983) studied hypomethylation in colon cancer and found that there was significant epigenetic modification of DNA

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Vijay K Gonugunta
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Lu Miao
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Gangadhara R Sareddy Department of Urology UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard J8130, Dallas, Texas 75390, USA

Department of Obstetrics and Gynecology UT Health Science Center, San Antonio, Texas, USA

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Preethi Ravindranathan
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Ratna Vadlamudi Department of Urology UT Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard J8130, Dallas, Texas 75390, USA

Department of Obstetrics and Gynecology UT Health Science Center, San Antonio, Texas, USA

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Ganesh V Raj
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regulation, transcription, cytoskeletal and epigenetic modifications, and ribosome biogenesis ( Choi et al . 2004 , Nair et al . 2007 , 2010 a , Chakravarty et al . 2010 a , 2011 , Gonugunta et al . 2011 , Mann et al . 2013 ). PELP1 is widely

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