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c-Myc Promotes Survival of WEHI 231 B Lymphoma Cells from Apoptosis

  • M. Wu
  • W. Yang
  • R. E. Bellas
  • S. L. Schauer
  • M. J. FitzGerald
  • H. Lee
  • G. E. Sonenshein
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 224)

Abstract

The c-myc oncogene has been implicated in control of cell proliferation, differentiation, as well as neoplastic transformation. More recently, overexpression or inappropriate time of expression of the c-myc gene has been found to promote apoptosis. Cleveland and coworkers observed that addition of a vector expressing c-Myc protein accelerated apoptosis following IL-3 deprivation of the 32D Independent myeloid cell line [3]. Similarly Evan and coworkers [10] found that transfection of 3T3 fibroblast cells with c-myc expression vectors led to enhanced levels of apoptosis upon growth arrest either by serum or isoleucine deprivation, or a thymidine block. These findings have been further extended using c-myc antisense oligonucleotides. Green and coworkers have shown that addition of these oligonucleotides to immature T cells and some T cell hybridomas, inhibited c-myc expression and prevented T cell receptor mediated apoptosis [23]. Together these results strongly suggest that inappropriate overexpression of c-myc promotes apoptosis in some cell systems.

Keywords

Myeloid Cell Line Burkitt Lymphoma Line Isoleucine Deprivation 
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

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • M. Wu
    • 1
  • W. Yang
    • 1
  • R. E. Bellas
    • 1
  • S. L. Schauer
    • 2
  • M. J. FitzGerald
    • 1
  • H. Lee
    • 1
  • G. E. Sonenshein
    • 1
  1. 1.Department of BiochemistryUniversity School of MedicineBostonUSA
  2. 2.Department of MicrobiologyUniversity School of MedicineBostonUSA

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