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Masaki Shiota Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Momoe Itsumi Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Ario Takeuchi Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Kenjiro Imada Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan
Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Akira Yokomizo Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Hidetoshi Kuruma Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Junichi Inokuchi Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Katsunori Tatsugami Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Takeshi Uchiumi Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Yoshinao Oda Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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Seiji Naito Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan

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recognizes N-terminus of AR protein and Twist1 (sc-81417) were purchased from Santa Cruz Biotechnology. Anti-phosphorylated Smad2/3 (p-Smad2/3; #8828) and anti-Smad2/3 (#8685) antibodies were obtained from Cell Signaling Technology (Cambridge, MA, USA

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R Formosa Department of Medicine, Department of Applied Biomedical Science, Neuroendocrine Clinic, Faculty of Medicine and Surgery, Mater Dei Hospital, University of Malta, Block A, Level 0, Msida MSD2080, Malta

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A Xuereb-Anastasi Department of Medicine, Department of Applied Biomedical Science, Neuroendocrine Clinic, Faculty of Medicine and Surgery, Mater Dei Hospital, University of Malta, Block A, Level 0, Msida MSD2080, Malta

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J Vassallo Department of Medicine, Department of Applied Biomedical Science, Neuroendocrine Clinic, Faculty of Medicine and Surgery, Mater Dei Hospital, University of Malta, Block A, Level 0, Msida MSD2080, Malta
Department of Medicine, Department of Applied Biomedical Science, Neuroendocrine Clinic, Faculty of Medicine and Surgery, Mater Dei Hospital, University of Malta, Block A, Level 0, Msida MSD2080, Malta

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. 2012 ). In this study, the effect of over-expressing and knocking down AIP proteins directly on cAMP signalling and GH secretion in the GH3 cell line was analysed. We provide evidence that AIP limits cAMP signalling and this in turn effects GH secretion

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Matthew Saldana Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA

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Kacey VanderVorst Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA

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Anastasia L Berg Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA

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Hyun Lee Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA

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Kermit L Carraway III Department of Biochemistry and Molecular Medicine, UC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Sacramento, California, USA

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TGFb, binding to their cognate cell-surface receptors. This stimulates the phosphorylation of the SMAD2 and SMAD3 transcription factors, which complex with SMAD4 and translocate to the nucleus to stimulate the transcription of target genes ( Massague

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Jun-ichiro Suzuki Faculty of Pharmacy, Musashino University, 1-1-20 Shin-machi, Nishitokyo-shi, Tokyo 202-8585, Japan

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Yasuko Murakami Faculty of Pharmacy, Musashino University, 1-1-20 Shin-machi, Nishitokyo-shi, Tokyo 202-8585, Japan

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Keijiro Samejima Faculty of Pharmacy, Musashino University, 1-1-20 Shin-machi, Nishitokyo-shi, Tokyo 202-8585, Japan

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Kohfuku Kohda Masahiro Ohtani Faculty of Pharmacy, Musashino University, 1-1-20 Shin-machi, Nishitokyo-shi, Tokyo 202-8585, Japan

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Takami Oka Faculty of Pharmacy, Musashino University, 1-1-20 Shin-machi, Nishitokyo-shi, Tokyo 202-8585, Japan

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Introduction Alpha cell differentiation and glucagon gene expression are mediated by multiple transcriptional factors including Pax6 ( St-Onge et al . 1997 ), ISL1 ( Wang & Drucker 1995 ), Cdx-2/3 ( Andersen et al . 1999 , Ritz-Laser et al

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Sayantani Sarkar
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Chandan Mandal
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Rajender Sangwan Cancer Biology and Inflammatory Disorder Division, Bio-Processing Unit, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology, 4, Raja S.C. Mallick Road, Kolkata 700032, West Bengal, India

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Chitra Mandal
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-dependent manner, which further promoted G2/M cell-cycle arrest. In addition to the MIAPaCa2 and BxPC3 cells, two other cell lines were also assessed based on their CDKN2A and SMAD4 mutational status, AsPC1 cells (a highly aggressive metastatic pancreatic tumor

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Rhonda L Bitting Divisions of Medical Oncology and Urology, Duke Cancer Institute, Duke University, DUMC Box 102002, Durham, North Carolina 27710, USA

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Andrew J Armstrong Divisions of Medical Oncology and Urology, Duke Cancer Institute, Duke University, DUMC Box 102002, Durham, North Carolina 27710, USA

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with metastatic CRPC, the survival rate of patients with metastatic CRPC remains poor and additional therapeutic approaches are needed. The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is a key oncogenic

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Isadora Pontes Cavalcante Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Anna Vaczlavik Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Ludivine Drougat Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Claudimara Ferini Pacicco Lotfi Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil

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Karine Perlemoine Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Christopher Ribes Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Marthe Rizk-Rabin Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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Eric Clauser Université de Paris, PARCC, INSERM, Paris, France

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Maria Candida Barisson Villares Fragoso Adrenal Unit, Hormone and Molecular Genetic Laboratory/LIM42, Hospital of Clinics, School of Medicine, University of São Paulo, São Paulo, Brazil

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Jérôme Bertherat Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France
Department of Endocrinology, APHP, Cochin Hospital, Paris, France

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Bruno Ragazzon Université de Paris, Institut Cochin, INSERM, CNRS, Paris, France

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-Rabin M Assie G Groussin L Fierrard H Perlemoine K Martinez A Bertherat J 2009 Inactivation of the Carney complex gene 1 (protein kinase A regulatory subunit 1A) inhibits SMAD3 expression and TGF beta-stimulated apoptosis in adrenocortical

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Sara Molatore Institute for Diabetes and Cancer, Helmholtz Zentrum München, Neuherberg, Germany

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Andrea Kügler Institute for Diabetes and Cancer, Helmholtz Zentrum München, Neuherberg, Germany

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Martin Irmler Institute of Experimental Genetics, Helmholtz Zentrum München, Neuherberg, Germany

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Tobias Wiedemann Institute for Diabetes and Cancer, Helmholtz Zentrum München, Neuherberg, Germany

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Frauke Neff Institute of Experimental Genetics, Helmholtz Zentrum München, Neuherberg, Germany

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Annette Feuchtinger Research Unit Analytical Pathology, Helmholtz Zentrum München, Neuherberg, Germany

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Johannes Beckers Institute of Experimental Genetics, Helmholtz Zentrum München, Neuherberg, Germany
German Center for Diabetes Research (DZD), Neuherberg, Germany
Technische Universität München, Chair of Experimental Genetics, Freising, Germany

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Mercedes Robledo Hereditary Endocrine Cancer Group, Spanish National Cancer Research Centre (CNIO) and ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Madrid, Spain

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Federico Roncaroli Division of Neuroscience and Experimental Psychology, Faculty of Medicine, University of Manchester, Manchester, UK

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Natalia S Pellegata Institute for Diabetes and Cancer, Helmholtz Zentrum München, Neuherberg, Germany

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Pde7b Phosphodiesterase 7B 10717069 −2.0 −3.78 PDE7B Steap2 STEAP family member 2, metalloreductase 10853401 −1.6 −3.66 STEAP2 Smad9 SMAD family member 9 10815436 −3.8 −3.62 SMAD9 Snta1 Syntrophin

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Xiaoli Liu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Chunhai Zhang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Xiaomiao Wang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Can Cui Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Hanwen Cui Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Baishu Zhu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Anqi Chen Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Lu Zhang Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Jingwei Xin Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Qingfeng Fu Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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Gianlorenzo Dionigi Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy
Division of Surgery, Istituto Auxologico Italiano, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy

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Hui Sun Division of Thyroid Surgery, China-Japan Union Hospital of Jilin University, Jilin Provincial Key Laboratory of Surgical Translational Medicine, Changchun, Jilin, China

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, as described previously ( Zhang et al. 2017 b ). Antibodies against TGFBR2 (mouse mAb, Cat#: 66636-1-Ig, 1:2000), USP15 (Mouse mAb, Cat#: 67557-1-Ig, 1:5000) and phosphorylated SMAD3 (Rabbit mAb, Cat#: ab52903, 1:5000) were purchased from

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Andreas Venizelos K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Hege Elvebakken Department of Oncology, Ålesund Hospital, Møre og Romsdal Hospital Trust, Ålesund, Norway
Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway

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Aurel Perren Institute of Pathology, University of Bern, Bern, Switzerland

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Oleksii Nikolaienko K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Wei Deng K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Inger Marie B Lothe Department of Pathology, Oslo University Hospital, Oslo, Norway

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Anne Couvelard Department of Pathology, Université de Paris, Bichat Hospital, AP-HP, Paris, France

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Geir Olav Hjortland Department of Oncology, Oslo University Hospital, Oslo, Norway

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Anna Sundlöv Departmentt of Oncology, Skåne University Hospital, Lund, Sweden
Department of Medical Radiation Physics, Lund University, Lund, Sweden

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Johanna Svensson Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Harrish Garresori Department of Oncology, Stavanger University Hospital, Stavanger, Norway

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Christian Kersten Department of Research, Hospital of Southern Norway, Kristiansand, Norway

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Eva Hofsli Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway
Department of Oncology, St.Olavs Hospital, Trondheim, Norway

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Sönke Detlefsen Department of Pathology, Odense University Hospital, Odense, Denmark
Department of Clinical Medicine, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark

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Merete Krogh Department of Oncology, Odense University Hospital, Odense, Denmark

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Halfdan Sorbye Department of Oncology, Haukeland University Hospital, Bergen, Norway
Department of Clinical Science, University of Bergen, Bergen, Norway

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Stian Knappskog K.G. Jebsen Center for Genome-Directed Cancer Therapy, Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Oncology, Haukeland University Hospital, Bergen, Norway

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Table 1). A prediction model for the classification of tumours into the categories LC-NEC or NET G3 was built, based on mutational status of nine genes ( APC , ATRX , BRAF , DAXX , KRAS , MEN1 , MYO5B , SMAD2 and TP53 ). Classification was

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