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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
Department of Urologic Sciences, Faculty of Medicine, University of British Columbia, British Columbia, Canada
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Department of Urologic Sciences, Faculty of Medicine, University of British Columbia, British Columbia, Canada
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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
Université de Paris, Paris, France
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Department of Nuclear Medicine, Sorbonne University, Pitie-Salpetriere Hospital, Paris, France
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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
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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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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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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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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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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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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, 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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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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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
University College London Cancer Institute, Neuroendocrine Tumour Unit, 72 Huntley Street, London WC1E 6BT, UK
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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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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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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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Department of Obstetrics and Gynecology UT Health Science Center, San Antonio, Texas, USA
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Department of Obstetrics and Gynecology UT Health Science Center, San Antonio, Texas, USA
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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