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Modulations of the epithelial phenotype during embryogenesis and cancer progression

  • Chapter
Mammary Tumorigenesis and Malignant Progression

Part of the book series: Cancer Treatment and Research ((CTAR,volume 71))

Abstract

In this chapter, we develop the idea that in order to be able to detach from the primary tumor, invade, and metastasize to distant organs, carcinoma cells must modify their adhesive status and change their cytoskeletal organization. Interestingly, such modifications of cell adhesion and communication systems have been shown to occur during embryogenesis and particulary during migratory process of epithelial-mesenchymal transition (EMT). These embryonic events therefore could represent the prototype of epithelial cell dispersion. Eventually, cells may switch back to a stable epithelial phenotype state that involves local growth and maintenance of this differentiated state, in coordination with the local environment. The delicate modulation of this equilibrium on a specific cell population represents a basic mechanism of embryogenesis. A similar mechanism of epithelial cell plasticity may apply to cancer cells. In this chapter, we first discuss this balance during a well-documented case of induced EMT in a bladder carcinoma. Then we expand the review to examples of EMT occurring during embryogenesis. Finally, we review cancer metastasis, with a special emphasis on breast cancer.

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Authors
  1. Pierre Savagner
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  2. Brigitte Boyer
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  3. Ana Maria Valles
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  4. Jacqueline Jouanneau
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  5. Jean Paul Thiery
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Editors and Affiliations

  1. Lombardi Cancer Research Center, Georgetown University School of Medicine, Washington, DC, USA

    Robert B. Dickson  & Marc E. Lippman  & 

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Savagner, P., Boyer, B., Valles, A.M., Jouanneau, J., Thiery, J.P. (1994). Modulations of the epithelial phenotype during embryogenesis and cancer progression. In: Dickson, R.B., Lippman, M.E. (eds) Mammary Tumorigenesis and Malignant Progression. Cancer Treatment and Research, vol 71. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2592-9_12

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  • DOI: https://doi.org/10.1007/978-1-4615-2592-9_12

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