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Bcl-2: B Cell Life, Death and Neoplasia

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Mechanisms in B-Cell Neoplasia 1990

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 166))

Abstract

The t(14;18)(q32;q21) is the most common translocation associated with human lymphoid malignancies. Approximately 85% of follicular and 20% of diffuse B cell lymphomas possess this translocation (Fukuhara 1979, Yunis 1987). Follicular lymphoma is initially a low grade disease consisting of small resting B cells. Over time, a histologic conversion to diffuse large cell architecture and aggressive high grade lymphoma occurs frequently in patients (Horning 1989). Molecular cloning of the t(14;18) breakpoint revealed a putative proto-oncogene, Bcl-2 at 18q21 (Bakhshi 1985, Cleary 1985, Tsujimoto 1985). The translocation occurs early in pre B cell development during Ig gene rearrangement and juxtaposes Bcl-2 with the Ig heavy chain locus at 14q32 (Bakhshi 1987). This creates a Bcl-2-Ig fusion gene that is markedly deregulated resulting in inappropriately elevated levels of Bcl-2-Ig RNA and the 25 kd Bcl-2 protein (Graninger 1987, Seto 1988). Bcl-2 encodes a 25 kd integral membrane protein of an intracellular organelle (Hockenbery, submitted). We have taken several approaches to examining the functional role of Bcl-2 including overexpressing Bcl-2 in lymphoblastoid lines, growth factor dependent lines and transgenic mice.

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© 1990 Springer-Verlag Berlin Heidelberg

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Korsmeyer, S.J., McDonnell, T.J., Nunez, G., Hockenbery, D., Young, R. (1990). Bcl-2: B Cell Life, Death and Neoplasia. In: Potter, M., Melchers, F. (eds) Mechanisms in B-Cell Neoplasia 1990. Current Topics in Microbiology and Immunology, vol 166. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75889-8_26

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  • DOI: https://doi.org/10.1007/978-3-642-75889-8_26

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-75891-1

  • Online ISBN: 978-3-642-75889-8

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