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Faith Nutter Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Ingunn Holen Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Hannah K Brown Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Simon S Cross Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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C Alyson Evans Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Matthew Walker Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Robert E Coleman Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Jules A Westbrook Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Peter J Selby Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Janet E Brown Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre
Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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Penelope D Ottewell Academic Unit of Clinical Oncology, Academic Unit of Pathology, Leeds Institute of Molecular Medicine, Cancer Research UK (CR‐UK), and Yorkshire Cancer Research (YCR) Sheffield Cancer Research Centre

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-IV tumours at any point over a 30 day time period, mean tumour area of 4.4±1.1 mm 2 being recorded for MDA-P cells and 3.4±1.7 mm 2 for MDA-IV cells at 35 days ( Fig. 3 c). Genetic alterations associated with bone-homing Intravenous injection of MDA

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Ali S Alzahrani Department of Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia
Department of Molecular Oncology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Meshael Alswailem Department of Molecular Oncology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Alexandre Buffet Université Paris Cité, Inserm, Paris Centre de Recherche Cardiovasculaire (PARCC), Equipe Labellisée Ligue contre le Cancer, Paris, France
Département de Médecine Génomique des Tumeurs et des Cancers, Fédération de Génétique et de Médecine Génomique, Assistance Publique-Hôpitaux de Paris (AP-HP) Centre, Hôpital Européen Georges Pompidou, Paris, France

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Balgees Alghamdi Department of Molecular Oncology, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Lulu Alobaid Department of Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Osamah Alsagheir Department of Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Hindi Al-Hindi Department of Pathology and Laboratory Medicine, King Faisal Specialist Hospital & Research Centre, Riyadh, Saudi Arabia

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Karel Pacak Section on Medical Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA

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approximately additional 30% of PPGLs carry somatic or postzygotic pathogenic variants ( Fishbein et al. 2017 , Nölting et al. 2021 ). These genetic alterations have been classified into at least three clusters based on their gene expression profiles

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Tanner Freeman Department of Pathology, UPMC, Pittsburgh, Pennsylvania, USA

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Charit Taneja Division of Endocrinology and Metabolism, UPMC, Pittsburgh, Pennsylvania, USA

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N Paul Ohori Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Abigail I Wald Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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John Skaugen Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Linwah Yip Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Seungwon Kim Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Robert L Ferris Department of Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
UPMC Hillman Cancer Center, Department of Oncology, Pittsburgh, Pennsylvania, USA

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Marina N Nikiforova Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Somak Roy Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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Yuri E Nikiforov Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

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molecularly identified thyroidal metastasis of renal cell carcinoma and genetic alterations detected in FNAs by ThyroSeq testing. Case Age (y); gender Nodule size (cm) BCC Cytologic features a Multiple nodules USG History of RCC

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Giovanna Maria Pierantoni
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Palma Finelli
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Emanuele Valtorta
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Daniela Giardino
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Ornella Rodeschini
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Francesco Esposito
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Marco Losa
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Alfredo Fusco
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Lidia Larizza
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-functioning pituitary adenomas (NFPAs). The genesis of pituitary tumors is still under investigation since the genetic alterations of the pituicytes themselves, hypothalamic dysregulation and locally produced growth factors have not been integrated in a multistep model

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Glenn T G Chang
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Mila Jhamai
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Wytske M van Weerden
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Guido Jenster
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Albert O Brinkmann
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-repressible apoptosis gene. Apoptosis 7 13 –21. Cher ML , Bova GS, Moore DH, Small EJ, Carroll PR, Pin SS, Epstein JI, Isaacs WB & Jensen RH 1996 Genetic alterations in untreated metastases and androgen-independent prostate cancer

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Angel Chao Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Huei-Jean Huang Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Chiao-Yun Lin Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Chia-Hwa Lee Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Chien-Hsing Lin Taiwan Genomic Industry Alliance Inc., Taipei, Taiwan

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An-Shine Chao Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Department of Obstetrics and Gynecology, New Taipei Municipal Tu Cheng Hospital, New Taipei City, Taiwan

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Chyong-Huey Lai Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Ting-Chang Chang Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Kai-Yun Wu Department of Obstetrics and Gynecology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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Ren-Chin Wu Gynecologic Cancer Research Center, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan
Department of Anatomic Pathology, Linkou Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Taoyuan, Taiwan

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patients (#SCT-01 and #SCT-03) had negative results on the TSO500 assay and underwent confirmatory testing with WES. The genetic alterations identified in the seven SCTs NOS samples are summarized in Table 2 . In brief, mutations in two hypoxia

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Arivarasan Karunamurthy Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Federica Panebianco Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Susan J Hsiao Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Jennie Vorhauer Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Marina N Nikiforova Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Simion Chiosea Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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Yuri E Nikiforov Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA

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encapsulated, is a typical phenotype of EIF1AX -mutated PTC. Since the follicular variant of PTC is known to share genetic alterations with other follicular-patterned thyroid tumors, that is, FTC and FA ( Nikiforov & Nikiforova 2011 ), it was important to

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David Viola Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Laura Valerio Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Eleonora Molinaro Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Laura Agate Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Valeria Bottici Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Agnese Biagini Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Loredana Lorusso Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Virginia Cappagli Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Letizia Pieruzzi Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Carlotta Giani Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Elena Sabini Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Paolo Passannati Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Luciana Puleo Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Antonio Matrone Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Benedetta Pontillo-Contillo Diagnostic and Interventional Radiology, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy

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Valentina Battaglia Diagnostic and Interventional Radiology, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy

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Salvatore Mazzeo Diagnostic and Interventional Radiology, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy

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Paolo Vitti Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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Rossella Elisei Department of Clinical and Experimental Medicine, Section of Endocrinology, University of Pisa, Pisa, Italy

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-RAS mutations are found in a relatively small percentage of PTCs, they represent the most frequent genetic alterations in FTCs, and they are also significantly present in PDTCs and ATCs ( Xing 2013 ). Other common genetic alterations in FTCs are PTEN deletion

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Sunmi Park Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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Mark C Willingham Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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Jun Qi Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, USA

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Sheue-Yann Cheng Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA

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reported that genetic alterations in the PI3K-AKT pathway play a critical role in thyroid tumorigenesis and progression ( Hou et al . 2007 , Wang et al . 2007 , Xing 2010 ). Furthermore, association of PTEN methylation with the activating genetic

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Thomas J Giordano Divisions of Anatomic Pathology and Molecular & Genomic Pathology, Departments of Pathology and Internal Medicine, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA

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of tumor classification schemes. Together with the identification of novel genetic alterations, these results have profound implications for the treatment of cancer patients. Tumors of endocrine organs are similarly genomic diseases. Compared to

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