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Oncogenes and Tyrosine Kinase Activities as a Function of the Metastatic Phenotype

  • Lea Eisenbach
  • Michael Feldman
Part of the NATO ASI Series book series (NSSA, volume 120)

Abstract

Cancer cell dissemination resulting in metastasis formation is a multistage process. It involves detachment of cells from the primary tumor (1), penetration of tumor cells through the host’s intercellular matrices and capillary basement membranes (2), dissemination via the blood circulation, extravasation into the target organ (3), and progressive growth in the target organs (4). At each of these steps the interaction between the disseminating cells and the host’s immune system may determine the probability of survival of the disseminating tumor cells. The generation of new antigenic variants (5) that are resistant to natural killer cells (6) or to cytotoxic T cells (7,8) was demonstrated in many tumor systems. We have shown that changes in the expression of genes of the major histocompatibility complex (MHC) control the immunogenicity and thereby the metastatic phenotype of individual clones of two murine tumors, the Lewis lung carcinoma and the T10 sarcoma (9–12). Are the immunogenic properties the only one to play a role in the metastatic phenotype or do other mechanisms play a role in the metastatic process of these two tumors? To explore additional components which control the metastatic phenotype of 3LL and T10 clones we tested the generation of metastases in the absence of an active immune system.

Keywords

Lewis Lung Carcinoma Disseminate Tumor Cell Metastatic Phenotype Plasma Membrane Vesicle Plasminogen Activator Activity 
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

© Plenum Press, New York 1986

Authors and Affiliations

  • Lea Eisenbach
    • 1
  • Michael Feldman
    • 1
  1. 1.Department of Cell BiologyThe Weizmann Institute of ScienceRehovotIsrael

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