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Latent cellular oncogenes: the paradox dissolves.

P H Duesberg1

  • 1Department of Molecular Biology, University of California, Berkeley 94720.

Journal of Cell Science. Supplement
|January 1, 1987
PubMed
Summary

Viral oncogenes are not simply transduced cellular cancer genes. Instead, they are genetic hybrids, and proto-oncogenes are not latent cancer genes, challenging existing cancer gene hypotheses.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Retroviral oncogenes are derived from cellular proto-oncogenes.
  • A prevailing hypothesis suggests proto-oncogenes act as latent cancer genes, activated within cells to cause tumors.

Purpose of the Study:

  • To critically evaluate the hypothesis that proto-oncogenes are latent cellular oncogenes.
  • To investigate the origin and nature of viral oncogenes and their cellular counterparts.

Main Methods:

  • Comparative sequence analysis of viral oncogenes, essential retroviral genes, and proto-oncogenes.
  • Examination of proto-oncogene expression in normal cells.
  • Analysis of cellular transformation assays using activated proto-oncogenes.
  • Review of tumor cell genetics, including chromosomal abnormalities.

Main Results:

  • Viral oncogenes are novel genetic hybrids, not direct transductions of cellular cancer genes.
  • Proto-oncogenes are commonly expressed in normal cells.
  • Activated proto-oncogenes have not transformed diploid cells in transfection experiments.
  • Diploid tumors with activated proto-oncogenes have not been identified.

Conclusions:

  • The hypothesis of proto-oncogenes as latent cellular oncogenes is an over-interpretation of sequence homology.
  • Rare genetic alterations, such as truncations and recombinations, likely generate viral and cellular cancer genes.
  • Clonal chromosomal abnormalities in tumor cells suggest rearrangements that may generate cancer genes, supporting Boveri's early tumor initiation theory.

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