Cellular Mortality, Growth Regulation, and the Phenomenon of Cancerous Transformation

  • Milton H. SaierJr.
  • Gary R. Jacobson

Abstract

Over the past few decades a huge research effort has been devoted to understanding the mechanisms of cancerous transformation. This effort has led to recognition of the fact that the unrestricted growth of most cancer cells is caused by release of normal cells within the body from the regulatory constraints imposed upon them. An understanding of cancerous transformation therefore leads to knowledge of the events controlling normal cell proliferation. In this chapter we shall first discuss the possible evolutionary origins of differentiated animal cells, both somatic (tissue) cells and germ (reproductive) cells. Subsequently, we shall consider the events that occur when normal cells become cancerous. It will become apparent that two distinct events frequently (but not always) accompany the transformation process: loss of sensitivity to growth regulation, and loss of the constraints of cellular mortality. Further, these two events are clearly distinct from each other, as well as from the genetic events that determine expression of the differentiated state. Although the phenomenon of cell mortality sometimes referred to as programmed cell death is presently poorly understood, it seems to have evolved as the terminal step in a sequence of irreversible differentiation events.

Keywords

Migration Lymphoma Tyrosine Leukemia Recombination 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

Selected References

  1. Bishop, J.M. Enemies within: the genesis of retrovirus oncogenes,Cell 23:5 (1981).PubMedCrossRefGoogle Scholar
  2. Brugge, J.S. and R.L. Erikson. Identification of a transformation-specific antigen induced by an avian sarcoma virus, Nature (London) 269:344 (1977).CrossRefGoogle Scholar
  3. Collett, M.S., A.F. Purchio, and R.L. Erikson. Avian sarcoma virus-transforming protein, pp60src shows protein kinase activity specific for tyrosine, Nature (London) 285:167 (1980).CrossRefGoogle Scholar
  4. Cooper, G.M. Cellular transforming genes, Science 277:801 (1982).CrossRefGoogle Scholar
  5. Koprowski, H., ed. Neoplastic Transformation: Mechanisms and Consequences, Life Sciences Research Report 7, Dahlem Workshop, Berlin, 1977.Google Scholar
  6. Martin, G.R. Teratocarcinomas as a model system for the study of embryogenesis and neoplasia, Cell 5:229 (1975).PubMedCrossRefGoogle Scholar
  7. Mintz, B. and K. Illmensee. Normal genetically mosaic mice produced from malignant teratocarcinoma cells, Proc. Natl. Acad. Sci USA 72:3585 (1975).PubMedCrossRefGoogle Scholar
  8. Pastan, I. and M. Willingham. Cellular transformation and the “morphologic phenotype” of transformed cells, Nature 274:645 (1978).PubMedCrossRefGoogle Scholar
  9. Saier, M.H. Jr., S. Erlinger and P. Boerner. “Studies on Growth Regulation and the Mechanism of Transformation of the Kidney Epithelial Cell Line, MDCK: Importance of Transport Function to Growth,” in Membranes in Growth and Development, Alan R. Liss Inc., New York, 1982:Google Scholar
  10. Stiles, C.D., W. Desmond, L.M. Chuman, G. Sato, and M.H. Saier, Jr. Growth control of heterologous tissue culture cells in the congenitally athymic nude mouse, Cancer Res. 56:1353 (1976).Google Scholar
  11. Stiles, C.D., W. Desmond, L.H. Chuman, G. Sato, and M.H. Saier, Jr. Relationship of cell growth behavior in vitro to tumorigenicity in athymic nude mice,Cancer Res. 36:3300 (1976).PubMedGoogle Scholar

Copyright information

© Springer-Verlag New York Inc. 1984

Authors and Affiliations

  • Milton H. SaierJr.
    • 1
  • Gary R. Jacobson
    • 2
  1. 1.Department of BiologyThe John Muir College University of California at San DiegoLa JollaUSA
  2. 2.Department of BiologyBoston UniversityBostonUSA

Personalised recommendations