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

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C-Myc in B-Cell Neoplasia

Part of the book series: Current Topics in Microbiology and Immunology ((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.

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© 1997 Springer-Verlag Berlin Heidelberg

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Wu, M. et al. (1997). c-Myc Promotes Survival of WEHI 231 B Lymphoma Cells from Apoptosis. In: Potter, M., Melchers, F. (eds) C-Myc in B-Cell Neoplasia. Current Topics in Microbiology and Immunology, vol 224. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60801-8_9

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  • DOI: https://doi.org/10.1007/978-3-642-60801-8_9

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-64560-0

  • Online ISBN: 978-3-642-60801-8

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