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      Origin and Progression of Thyroid Epithelial Tumours: Cellular and Molecular Mechanisms

      Hormone Research in Paediatrics

      S. Karger AG

      ras, ret, gsp, Thyroid-stimulating hormone, Thyroid, Oncogene, Tumour-suppressor gene, Differentiation, p53

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          Abstract

          Tumours of the thyroid follicular cell are proving to be one of the most informative models for ‘dissecting’ the molecular genetics of multi-stage human tumorigenesis. Early thyroid tumour development is closely correlated with mutation of five alternative genes, ras, ret, trk, gsp and the TSH receptor, associated with different tumour phenotypes, providing an excellent example of genotype/phenotype correlation. For two of these genes, ras and ret, there is also direct experimental evidence from gene transfer studies that they are sufficient to initiate tumorigenesis, one of very few situations where such proof of causality has been obtained for a human tumour. Much less is known of the molecular basis of malignant transformation in thyroid. However, the rare, further progression to undifferentiated (anaplastic) cancer provides a particularly clear-cut illustration of the role of the tumour-suppressor gene p53 in human cancer. Furthermore, in vitro data suggest the intriguing possibility that the anaplastic phenotype results from a combination of p53 mutation together with a spontaneous switch in differentiation programme, i.e. co-operation between a genetic and an epigenetic event.

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          Author and article information

          Journal
          HRE
          Horm Res Paediatr
          10.1159/issn.1663-2818
          Hormone Research in Paediatrics
          S. Karger AG
          978-3-8055-6504-2
          978-3-318-01928-5
          1663-2818
          1663-2826
          1997
          1997
          09 December 2008
          : 47
          : 4-6
          : 145-157
          Affiliations
          Cancer Research Campaign Thyroid Tumour Biology Group, Department of Pathology, University of Wales College of Medicine, Cardiff, UK
          Article
          185458 Horm Res 1997;47:145–157
          10.1159/000185458
          9167946
          © 1997 S. Karger AG, Basel

          Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

          Page count
          Pages: 13
          Categories
          Recent Progress on the Molecular Aspects of Endocrine Tumors: Clinical Implications

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