By F. Melchers, D. Haasner, H. Karasuyama, L. Reininger, A. Rolink (auth.), Michael Potter M. D, Prof. Dr. Fritz Melchers (eds.)
Major issues coated: B-Cell improvement; Immunoglobulin Gene Rearrangement; a number of Myeloma, Plasmactomas; Lymphomas: B-CLL, Folli- cular Lymphomas BCL-2, BCL-1; Lymphomas: EBV, AIDS Associa- ted Lymphomas; Oncogenes and Transcriptional elements (text to stick with)
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Extra resources for Mechanisms in B-Cell Neoplasia 1992: Workshop at the National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, April 21–23, 1992
1992). It is also true. however. that some inconsistency is still present among the previous results on the growth signal requirement of B precursors. Given that control of cell proliferation in higher organisms might be achieved in a redundant and failsafe manner. this redundancy could be a source of the inconsistency among the previous results. Thus. in this article. we would like to re-examine three key propositions which we have been stated in the previous studies and discuss them in detail in light of the previous results of ours and other groups.
1988), and oligodendrocytes (McMorris et al. 1986). l_ _ _~> Plunpol8nt SlemCall P.... P.... Cell CeNtl < IL-7 PnI-8 Cell IL-7+IGF-1 IL-7+KL _. • eel CeRIl >--- Prolnera1ion Signals Fig. l. A model of primary B cell development. Dashed lines indicate that the placement of developmental or proliferative signals is approximate. Ig gene rearrangement events are placed at the cellular stage at which they first occur. Whether IGF-I acts to directly stimulate differentiation or is a survival factor that allows cells to progress through a stochastic program of development is not clear_ A hallmark of B cell development is that there is extensive expansion of the progenitor cell pool, but IGF-I alone does not appear to mediate this activity.
On initial analysis, this observation seemed at odds with the findings in which S17 cells supported the generation of surface IgM expressing cells in long-term bone marrow cultures. However, the latter study could not distinguish if S17 cells directly supported the generation of surface IgM expressing B cells or other accessory cell populations, such as macrophages (Kincade et al. 1981), present in the cultures That the S17 line does not support the development of Ig light chain expressing cells was substantiated by Henderson et al.