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Endocrine Genetics Unit LIM-25, Neuroendocrinology Unit, Adrenal Unit (LIM-42), Experimental Oncology Laboratory (LIM-24), Nursing School, School of Public Health, Endocrinology Division, Brigadeiro Hospital, Federal University of Sao Paulo, Human Genome Research Center, Department of Cell and Developmental Biology, Instituto do Cérebro, National Institute of Aging, Institute of Pathology, School of Medicine, Hospital das Clinicas, University of Sao Paulo, Sao Paulo, Brazil
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Endocrine Genetics Unit LIM-25, Neuroendocrinology Unit, Adrenal Unit (LIM-42), Experimental Oncology Laboratory (LIM-24), Nursing School, School of Public Health, Endocrinology Division, Brigadeiro Hospital, Federal University of Sao Paulo, Human Genome Research Center, Department of Cell and Developmental Biology, Instituto do Cérebro, National Institute of Aging, Institute of Pathology, School of Medicine, Hospital das Clinicas, University of Sao Paulo, Sao Paulo, Brazil
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, SDHC , SDHD , SDHAF2 , PRKAR1A , AIP , TMEM127 , MAX , p15 INK4B ( CDKN2A ), p18 INK4C ( CDKN2C ), p21 CIP1 ( CDKN1A ), and p27 Kip1 ( CDKN1B )) and two protooncogenes ( RET and HIF2A ( EPAS1 )) ( Pellegata et al . 2006 , Agarwal et
Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Istituto dei Tumori di Napoli Fondazione ‘G. Pascale’, Dipartimento di Medicina Sperimentale e Clinica, Inflammation Research, NOGEC (Naples Oncogenomic Center)-Ceinge, Via S. Pansini 5, 80131 Naples, Italy
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Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Istituto dei Tumori di Napoli Fondazione ‘G. Pascale’, Dipartimento di Medicina Sperimentale e Clinica, Inflammation Research, NOGEC (Naples Oncogenomic Center)-Ceinge, Via S. Pansini 5, 80131 Naples, Italy
Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Istituto dei Tumori di Napoli Fondazione ‘G. Pascale’, Dipartimento di Medicina Sperimentale e Clinica, Inflammation Research, NOGEC (Naples Oncogenomic Center)-Ceinge, Via S. Pansini 5, 80131 Naples, Italy
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et al . 2000 ), and alterations of the p27 kip protein function ( Baldassarre et al . 1999 ) represent frequent features of thyroid malignancies. p27 kip1 has classically been regarded as a cell-cycle inhibitor based on its potent inhibitory
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bioinformatic programs miRGen ( www.diana.pcbi.upenn.edu/miRGen ; Megraw et al. 2007 ), TargetScan ( Lewis et al. 2003 ), Pictar ( Krek et al. 2005 ), and miRanda ( John et al. 2004 ) to predict human miR gene targets, we identified the CDKN1B ( p27
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Hereditary Endocrine Cancer Group, University Magna Graecia, Institute for Genetic Research IRGS, Genotyping Unit, ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Human Cancer Genetics Programme, Spanish National Cancer Centre, Centro Nacional de Investigaciones Oncológicas (CNIO), Calle Melchor Fernández Almagro, 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, University Magna Graecia, Institute for Genetic Research IRGS, Genotyping Unit, ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Human Cancer Genetics Programme, Spanish National Cancer Centre, Centro Nacional de Investigaciones Oncológicas (CNIO), Calle Melchor Fernández Almagro, 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, University Magna Graecia, Institute for Genetic Research IRGS, Genotyping Unit, ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Human Cancer Genetics Programme, Spanish National Cancer Centre, Centro Nacional de Investigaciones Oncológicas (CNIO), Calle Melchor Fernández Almagro, 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, University Magna Graecia, Institute for Genetic Research IRGS, Genotyping Unit, ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Human Cancer Genetics Programme, Spanish National Cancer Centre, Centro Nacional de Investigaciones Oncológicas (CNIO), Calle Melchor Fernández Almagro, 3, 28029 Madrid, Spain
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Hereditary Endocrine Cancer Group, University Magna Graecia, Institute for Genetic Research IRGS, Genotyping Unit, ISCIII Center for Biomedical Research on Rare Diseases (CIBERER), Human Cancer Genetics Programme, Spanish National Cancer Centre, Centro Nacional de Investigaciones Oncológicas (CNIO), Calle Melchor Fernández Almagro, 3, 28029 Madrid, Spain
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encodes p27 Kip1 , an inhibitor of the cyclin/cyclin-dependent kinase (Cdk) complexes ( Sa et al . 2005 ), which are essential for cell cycle progression. Loss of expression of p27 Kip1 protein has been described as a frequent event in several human
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known as MEN4 (OMIM #610755). MEN4 is caused by germline mutations in Cdkn1b in rats and CDKN1B in humans, coding for p27 Kip1 (commonly referred to as p27 or KIP1, hereafter p27), a putative tumor suppressor gene regulating cell cycle progression
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pathological and molecular changes associated with therapy. Response to endocrine therapy Initially, 89 patients were recruited for treatment irrespective of oestrogen receptor (ER) status. However, only 1 of 27 ER-poor tumours (defined as
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German Center for Diabetes Research (DZD), Neuherberg, Germany
Technische Universität München, Chair of Experimental Genetics, Freising, Germany
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Introduction The cyclin-dependent kinase (CDK) inhibitor p27 is a negative regulator of the cell cycle. It is post-translationally downregulated in over 50% of human cancers and its low expression is an independent predictor of poor survival
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to replicate their DNA in low serum ( Zhang et al. 1995 , Sutterluty et al. 1999 ). Control of cell cycle progression by Skp2 has been linked to its ability to control the levels of the CDK inhibitor p27 ( Slingerland & Pagano 2000
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test and a theoretical mean of 1. Criterion for significance was P < 0.05. All data are presented as mean ± s.e.m . Results Enzymes that regulate bioavailability of 27-hydroxycholesterol and its cognate receptor LXR are expressed in EC
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Departments of, Endocrinology, Molecular Genetics, Institute of Pathology, Laboratory of Biochemistry and Molecular Biology, CRN2M, Department of Experimental Medicine, Neuromed, Division of Endocrinology, Department of Endocrinology, Group for Advanced Molecular Investigation, Service d'Endocrinologie, Department of Endocrinology, Unit of Endocrinology, Department of Endocrinology, Department of Endocrinology, Clinical Center of Endocrinology and Gerontology, Faculty of Medicine, Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Internal Medicine and Endocrinology, Department of Endocrinology, Service d'Endocrinologie, Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart‐Tilman, University of Liège, 4000 Liège, Belgium
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Departments of, Endocrinology, Molecular Genetics, Institute of Pathology, Laboratory of Biochemistry and Molecular Biology, CRN2M, Department of Experimental Medicine, Neuromed, Division of Endocrinology, Department of Endocrinology, Group for Advanced Molecular Investigation, Service d'Endocrinologie, Department of Endocrinology, Unit of Endocrinology, Department of Endocrinology, Department of Endocrinology, Clinical Center of Endocrinology and Gerontology, Faculty of Medicine, Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Internal Medicine and Endocrinology, Department of Endocrinology, Service d'Endocrinologie, Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart‐Tilman, University of Liège, 4000 Liège, Belgium
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Departments of, Endocrinology, Molecular Genetics, Institute of Pathology, Laboratory of Biochemistry and Molecular Biology, CRN2M, Department of Experimental Medicine, Neuromed, Division of Endocrinology, Department of Endocrinology, Group for Advanced Molecular Investigation, Service d'Endocrinologie, Department of Endocrinology, Unit of Endocrinology, Department of Endocrinology, Department of Endocrinology, Clinical Center of Endocrinology and Gerontology, Faculty of Medicine, Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Endocrinology, Department of Internal Medicine and Endocrinology, Department of Endocrinology, Service d'Endocrinologie, Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart‐Tilman, University of Liège, 4000 Liège, Belgium
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). Interest in the role of CDKN1B mutations in other endocrine-related cancer has risen, with a recent study showing that 2/86 sporadic parathyroid adenoma patients had germline CDKN1B mutations, which, in turn, affected p27 protein levels or stability