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, we examine the genetic and epigenetic links between autophagy and thyroid carcinogenesis. A better understanding of such mechanistic connections could help to identify new targets for a more accurate diagnostic, prognostic, and therapeutic management
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increasing evidence of OIS involvement in human cancer suggests the possibility of new therapeutic approaches based on the functional restoration of OIS in tumour cells. In this study, we investigate the occurrence of OIS in thyroid carcinogenesis with in
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emerged to play a fundamental role in thyroid carcinogenesis ( Paes & Ringel 2008 ). Since we observed an inhibitory impact of the PI3K/Akt pathway on FOXO3a activity in vitro , we were interested to know whether this regulatory principle might also apply
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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data show increased miR221 and 222 levels in PTCs that correlate with low levels of p27 ( Visone et al . 2007 ). However, a causal link between p27 impairment and thyroid carcinogenesis has not been established yet. The aim of the present work was to
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microenvironment is established in thyroid tumors and what is its influence on the outcome of patients with DTC. Principles of thyroid carcinogenesis Although ∼50–67% of the population will eventually present a thyroid nodule during their lives ( Mazzaferri 2006
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human thyroid cancer with a pathological progression from hyperplasia to capsular invasion, vascular invasion, and eventually metastasis ( Suzuki et al . 2002 ). Extensive molecular analyses of altered signaling pathways during thyroid carcinogenesis
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increased risk thyroid cancer, the molecular mechanisms by which obesity increase the risk of thyroid cancer progression are poorly understood. Because it would be difficult to study how obesity could affect thyroid carcinogenesis in patients at the
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Helmholtz Zentrum München – German Research Center for Environmental Health GmbH, Clinical Cooperation Group ‘Personalized Radiotherapy in Head and Neck Cancer’, Neuherberg, Germany
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Helmholtz Zentrum München – German Research Center for Environmental Health GmbH, Clinical Cooperation Group ‘Personalized Radiotherapy in Head and Neck Cancer’, Neuherberg, Germany
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Department of Radiation Oncology, University Hospital, LMU Munich, Munich, Germany
Helmholtz Zentrum München – German Research Center for Environmental Health GmbH, Clinical Cooperation Group ‘Personalized Radiotherapy in Head and Neck Cancer’, Neuherberg, Germany
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according to a multi-step model ( Vogelstein & Kinzler 1993 , Kondo et al. 2006 ). Those alterations, that consequently stimulate effectors of the MAPK signaling pathway or PI3K/AKT signaling pathway, play a central role in thyroid carcinogenesis
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IC Crystallography Institute, National Research Council, CNR, Catania, Italy
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) Nakashima M Suzuki K Meirmanov S Naruke Y Matsuu‐Matsuyama M Shichijo K Saenko V Kondo H Hayashi T Ito M , et al . 2008 Foci formation of P53‐binding protein 1 in thyroid tumors: activation of genomic instability during thyroid
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Our aims were to uncover the role of FAM172A (Family with sequence similarity 172 member A) in the pathogenesis of follicular thyroid carcinoma (FTC) and to evaluate its value in the differential diagnosis between malignant and benign thyroid follicular lesions. FAM172A expression was evaluated by q-PCR, immunoblotting and immunohistochemistry (IHC). The ability of proliferation, migration and invasion of cells were assessed by Cell Counting Kit-8 assay (CCK8), clone-formation and Transwell assays. Nude mouse tumorigenicity assays were used to investigate the role of FAM172A in the pathogenesis of FTC in vivo. The value of FAM172A in the differential diagnosis for FTC was assessed using 120 formalin-fixed paraffin-embedded (FFPE) tissues after the operation and 81 fine-needle aspiration biopsy (FNAB) samples before the operation. FAM172A was highly expressed in FTC tissues and FTC cell lines. Downregulation of FAM172A inhibited the proliferation, invasion and migration of FTC cells through Erk1/2 and JNK pathways. Subcutaneous tumorigenesis in nude mice showed that knockdown of FAM172A inhibited tumor growth and progression in vivo. The FAM172A IHC scores of 3.5 had 92% sensitivity and 63% specificity to separate FTC from benign/borderline thyroid follicular lesions, and 92% sensitivity and 80% specificity to discriminate FTC from benign thyroid follicular lesions in postoperative FFPE samples. The corresponding values were 75 and 78%, and 75 and 89% in preoperative FNA samples, respectively. FAM172A plays an important role in the pathogenesis of FTC through Erk1/2 and JNK pathways. FAM172A may be a potential marker for the preoperative diagnosis of FTC based on the IHC results of thyroid FNAB samples.