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Division of Endocrinology, University of Texas Medical Branch, Galveston, Texas, USA
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reported widespread DNA copy number alterations (CNA), typically leading to near complete genome haploidization, as a likely genetic mechanism of HCC ( Corver et al. 2012 ). This type of CNA involved multiple chromosomes with chromosome-wide monosomy and
Department of Oncology, Haukeland University Hospital, Bergen, Norway
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Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
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Department of Oncology, Haukeland University Hospital, Bergen, Norway
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Department of Oncology, Haukeland University Hospital, Bergen, Norway
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Department of Medical Radiation Physics, Lund University, Lund, Sweden
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Department of Oncology, St.Olavs Hospital, Trondheim, Norway
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Department of Clinical Medicine, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark
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Department of Clinical Science, University of Bergen, Bergen, Norway
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Department of Oncology, Haukeland University Hospital, Bergen, Norway
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molecular mechanisms and genetic origin of these tumours as well as why these cancers are so aggressive. Importantly, we reveal a high fraction of targetable alterations in HG GEP-NEN patients, pointing to novel treatment strategies applying tailored
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Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK
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). Furthermore, advanced-stage disease in most cases develops resistance to ADT, underscoring the unmet clinical need to develop new treatments for metastatic castration-resistant PCa (mCRPC). Although the effects of DNA repair defects and genetic
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Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan
Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
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inhibition showed similar effects as the genetic silencing of SREBF1 in thyroid cancer cells. Figure 4 Alterations in metabolism, cell morphology, and motility following treatment with fatostatin, an inhibitor of SREBP1 activation. BHT-101 and FTC
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intense TSH stimulation should be performed before any administration of 131 I in thyroid cancer patients. Furthermore, several alterations in the post-translational modification and targeting of NIS protein to the plasma membrane and in its degradation
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precursor, 7-dehydrocholesterol ( Leyssens et al. 2013 , Christakos et al. 2016 , 2019 , Jeon & Shin 2018 ). Since exposure to sunlight is a major trigger for vitamin D 3 synthesis in the skin, alterations in sunlight exposure based on season and
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and mRNA level ( Luo et al. 2006 , Dezső et al. 2008 ). Recently, a large pangenomic analysis of hepatoblastoma has revealed that upregulation of imprinted genes from the 14q32 locus, including DLK1 , is a genetic hallmark of the malignancy