By D. G. Osmond, Y.-H. Park, K. Jacobsen (auth.), Michael Potter M.D., Prof. Dr. Fritz Melchers (eds.)
The papers during this publication have been offered on the sixth Workshop on Mechanisms in B-Cell Neoplasia, held in Bethesda, March 23-25, 1988. On trade years this assembly is backed through the . ;. Basel Institute of Immunology in Basel, Switzerland and by way of the nationwide melanoma Institute in Bethesda, and is attended by means of a hundred to a hundred and fifty parti cipants. This sixth workshop, just like the previous 5, used to be characterised by means of extreme and enthusiastic dialogue which displays, we expect, the interesting progress and improvement of this box. it's fairly transparent, even if, that regardless of many basic advances an realizing of the appropriate underlying mechanisms in B-cell tumor improvement isn't really but outlined. most likely, there isn't any unmarried mechanism for the entire a number of different types of B-cell neo plastic improvement. many various sorts of B-cell neoplasms are identified, and those are unique by means of a number of features: 1) the degree of improvement attained by means of the tumor stem cells; 2) mode of progress (slow or fast); three) organization with usual or inductive etiologic brokers and four) particular and constant mutational mechanisms reminiscent of retroviral insertion, chromosomal rearrangement. these charac teristic kinds which come up certainly in quite excessive frequency or these tumors with hallmark houses which might be caused regularly are the types most often studied, e. g. , endemic Burkitt's lymphoma, follicular lymphoma, acute and protracted lymphocytic leukemia and a number of myeloma in guy; bursal lymphoma in chickens; Abelson virus brought about pre B mobilephone lymphomas and plasmacytomas in mice and immunocytomas in rats. each one version process, has detailed difficulties and advantages.
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Additional info for Mechanisms in B-Cell Neoplasia 1988: Workshop at the National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, March 23–25, 1988
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J Exp Med 160:19011918. Molecular Characterization of a 1hmsforming Retrovirus Involved in Pre-B Cell Lymphomas W. Y. , J. W. HARTLEy2, S. P. , S. K. RUSCETTI3, and H. C. MORSE m2 INTRODUCTION Cas-Br-M is a biologically cloned ecotropic murine leukemia virus [MuLV] originally isolated from wild mice of the Lake Casitas region of California. Inoculation of Cas-Br-M into newborn NFS/N mice induces hematopoietic neoplasms. The tumors are evident at 18-30 weeks and include T- and B-cell lymphomas, myeloid leukemias and erythroleukemias [Fredrickson et aI, 1984].
Clark and o. witte, unpublished observations) . BIOLOGICAL ACTIVITIES OF THE BCR/ABL GENE PRODUCTS Although the correlation of the expression of P210 and P185 to CML and ALL provided a strong suggestion that they played a central role in the genesis of these leukemias, it was critical to test various in vitro tissue culture and in vivo animal models to assess their functional capabilities. -Complete cDNA copies of the coding sequences for the P210 protein (Mes-Masson et al 1986) were constructed into retrovirus vectors and expressed in murine 3T3 type fibroblastic cell lines (Daley, McLaughlin, witte & Baltimore 1987; McLaughlin, Chianese & Witte 1987) by transfection or infection.
In spite of their resemblance to macrophages, these cells were not phagocytic and they did not produce nonspecific esterase or lysozyme. In addition, they were negative for cytoplasmic mu chains by RIA. This overall lack of distinguishing characteristics made it impossible to assign these clones to any hematopoietic lineage. The second category, representative of pre-B cells, included only the J2C3 subc10ne 1. These cells were uniformly Ly-17(FcR)+, sIg-, and contained a subpopulation of Ly-5(B220)+ cells.