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Abrogation of IL-3 Dependence of Myeloid FDC-P1 Cells by Tyrosine Kinase Oncogenes Is Associated with Induction of c-myc

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Mechanisms in B-Cell Neoplasia 1988

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 141))

Abstract

A role for the c-myc proto-oncogene in growth factor signal transduction first came from experiments showing that the gene was inducible by treating quiescent T cells and fibroblasts with experimental mitogens or growth factors (Kelly et al., 1983). Subsequently, subtractive cDNA cloning from PDGF-treated fibroblast cells identified c-myc as an early Gl or competence gene in these cells (Cochran et al., 1983). Significance for this induction was established from studies demonstrating that introduction of constitutively expressed source of exogenous c-myc or microinjection of purified c-myc protein relieved the requirements for PDGF in the transition from GO into Gl (Armelin et al., 1984; Kaczmarek et al., 1985).

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© 1988 Springer-Verlag Berlin · Heidelberg

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Cleveland, J.L., Dean, M., Wang, J.Y., Hedge, AM., Ihle, J.N., Rapp, U.R. (1988). Abrogation of IL-3 Dependence of Myeloid FDC-P1 Cells by Tyrosine Kinase Oncogenes Is Associated with Induction of c-myc . In: Potter, M., Melchers, F. (eds) Mechanisms in B-Cell Neoplasia 1988. Current Topics in Microbiology and Immunology, vol 141. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74006-0_40

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  • DOI: https://doi.org/10.1007/978-3-642-74006-0_40

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-74008-4

  • Online ISBN: 978-3-642-74006-0

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