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The Use of cDNA Cloning Techniques to Isolate Genes Activated in Tumour Cells

  • M. R. D. Scott
  • P. M. Brickell
  • D. S. Latchman
  • D. Murphy
  • K.-H. Westphal
  • P. W. J. Rigby
Conference paper
Part of the Haematology and Blood Transfusion / Hämatologie und Bluttransfusion book series (HAEMATOLOGY, volume 28)

Abstract

Oncogenic transformation by tumour viruses requires, in many cases, the function of only one viral gene. In the case of the papovavirus Simian virus 40 (SV40) it is the gene coding for large T-antigen [8, 16] while for most strongly transforming retroviruses it is a gene of cellular origin [1]. Recent work has shown that many murine and human tumours, for which there is no indication of viral involvement, contain genes which have been altered in such a way that they have acquired the ability to transform the NIH3T3 line of mouse cells [3, 5, 7, 10, 15]. In order to understand the molecular mechanisms of oncogenesis it is necessary to analyse in detail the biochemical functions of the protein products of these various types of transforming gene. However, even a total description of the activities of a transforming protein will not reveal the complete mechanism of oncogenesis. Transformed cells differ from their normal parents in a multitude of biological and biochemical properties and it is unlikely that all of these changes occur as a direct result of the action of the transforming protein. Rather, the product of the oncogene must reprogramme the cell’s metabolism and/or gene expression so that having defined the transforming protein it is then necessary to identity its cellular targets.

Keywords

Mouse Cell Rous Sarcoma Virus Polyoma Virus NIH3T3 Line European Molecular Biology Organisation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1983

Authors and Affiliations

  • M. R. D. Scott
  • P. M. Brickell
  • D. S. Latchman
  • D. Murphy
  • K.-H. Westphal
  • P. W. J. Rigby

There are no affiliations available

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