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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
CEA, Department of Nuclear Medicine and Endocrine Oncology, Inserm, Institut Gustave Roussy, Université Paris XI, INSERM ERI-21, University of Nice-Sophia Antipolis, Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA Tumour/Tissue Bank of Nice Area, Department of Otorhinolaryngology, Institut Curie, CNRS, Université Paris VI, DSV, IRCM, LCE, BP6, Fontenay-aux-Roses F-92265, France
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some DNA mutations, we searched for RAS , RET/PTC , and BRAF genetic alterations in the learning/training set of tumors ( Tables 1 and 2 ). Mutations at codon 61 of NRAS , HRAS , or KRAS were found in one rFTA and two sFTA. RET
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that genetic alteration of the TP53 gene and dysregulated glucose metabolism partly involve low PR expression in ER-positive and HER2-negative breast cancer. Supplementary data This is linked to the online version of the paper at https
Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Laennec, UMR 664, Lyon F-69372, France
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Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Laennec, UMR 664, Lyon F-69372, France
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Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Laennec, UMR 664, Lyon F-69372, France
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Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Laennec, UMR 664, Lyon F-69372, France
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Bl/6 genetic background. The possibility of masked interferences between genetic alterations has been studied. We found that the level of expression of the E7 oncogene (data not shown) and the level of expression of RP3 oncogene ( Fig. 5 ) were
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clinical stigmata of CS, consistent with a mild glucocorticoid resistance syndrome. Genetics As discussed, PBMAH may be associated with genetic alterations of the ACTH receptor MC2R (extremely rare), PRKACA and PDE11A . Rarely, PBMAH may be
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neuroblastoma is rare and major susceptibility genes have not yet been isolated, many investigators have attempted to define the somatic genetic and epigenetic alterations associated with neuroblastoma development. Common genetic events include N
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single-base substitutions at the promoter of hTERT . Forty-six out of 49 genetic alterations found in coding regions are recorded in the COSMIC databases. The remaining three were not previously described in solid tumors and they were detected in AKT1
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-resolution analysis of genetic alterations in small bowel carcinoid tumors reveals areas of recurrent amplification and loss . Genes, Chromosomes and Cancer 47 591 – 603 . ( https://doi.org/10.1002/gcc.20561 ) 10.1002/gcc.20561 Kölby L Bernhardt P Ahlman H
Departments of Orthopaedic Surgery, Physiology and Biophysics, Radiation Oncology, Breast Cancer Research Program, Hematology and Oncology, Barton Research Institute, Center for Orthopaedic Research
Departments of Orthopaedic Surgery, Physiology and Biophysics, Radiation Oncology, Breast Cancer Research Program, Hematology and Oncology, Barton Research Institute, Center for Orthopaedic Research
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Departments of Orthopaedic Surgery, Physiology and Biophysics, Radiation Oncology, Breast Cancer Research Program, Hematology and Oncology, Barton Research Institute, Center for Orthopaedic Research
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Departments of Orthopaedic Surgery, Physiology and Biophysics, Radiation Oncology, Breast Cancer Research Program, Hematology and Oncology, Barton Research Institute, Center for Orthopaedic Research
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environmental pressure, heterogeneity in gene expression develops within the population of tumor cells, for example due to the effects of genomic instability and the accumulation of mutations and other genetic aberrations. Clonal selection then determines that
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between HIF-1 over-expression and poor patient outcome. The activity of HIF-1 is increased in response to intratumoural hypoxia and as a result of genetic alterations that activate oncogenes and inactivate tumour suppressor genes. HIF-1 plays a key role in
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excluded and has been attributed to either iodine supplementation ( Farahati et al . 2004 ) or exposure to radiation or other environmental endocrine disruptors, especially during childhood ( Tronko et al . 2006 ). Many genetic alterations have been