Do we understand the genetic mechanisms of oncogenesis? Keynote address for Honey Harbor meeting on cellular and molecular biology of neoplasia, October 2-6, 1983

J Cell Physiol Suppl. 1984:3:1-11. doi: 10.1002/jcp.1041210403.

Abstract

Different experiments with viruses and transfection now support the classical view that cancer is the result of a multistep process. This analysis further indicates that some of these steps involve mutations affecting the qualitative and quantitative expression of dominant transforming genes or oncogenes. These mutations are spontaneous or induced and of various kinds, including base pair changes, deletions, translocations, and amplifications. The actions of the active transforming genes or oncogenes lead to the properties of the tumor cell. However, these activities are effective only in the appropriate cell with targets for the products of the oncogenes and without inhibitors. Because there will be multiple genetic changes in tumor cells, it is difficult to determine which changes are significant for the oncogenesis. Retrovirus vectors may be useful in this determination. In addition, our present methods of analysis may be missing certain of the multiple steps in oncogenesis, in particular, those involved with tissue-, organ-, and organism-specific controls.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Base Sequence
  • Cell Transformation, Neoplastic*
  • Cell Transformation, Viral*
  • Models, Biological
  • Models, Genetic
  • Mutation
  • Oncogenes*
  • Recombination, Genetic
  • Retroviridae / genetics
  • Transfection
  • Virus Replication