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Oncogenes in B-Cell Neoplasia
Workshop at the National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, March 5-7, 1984
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Michael Potter, Fritz Melchers, Martin Weigert The second workshop on Mechanisms of B Cell Neoplasia was held in Bethesda, Maryland in Wilson Hall at the National Institutes of Health on March 5, 6, and 7, 1984. It followed a workshop on the same topic that was held at the Basel Institute for Immunology, March 15-17, 1983. That first meeting attempted to bring together cell biologists, experimental pathologists and molecular geneti cists interested in B cells, to discuss pathogenetic processes in the development and maintenance of the neoplastic state. The impetus for this discussion emanated from two important developments: first, the discovery of the viral promoter insertion mechanism for acti vating the myc oncogene in bursal lymphomatosis by Hayward, Neil, and Astrin;-second, the findings that the non-random chromosomal trans locations involving the immunoglobulin gene chromosomes occur red in very high frequencies in murine plasmacytomas and human Burkitt's lymphomas. During the planning stages of that meeting Shen-Ong et al. discovered that non-random translocations activated the myc oncogene. Promoter insertions and non-random trans locations were-rwo mechanisms that caused transcription of the myc oncogene messages in three different kinds of well defined experimental and clinical B cell tumors. Unregulated myc gene transcription provided the first evidence of a specific bioChemical lesion in B cell neo plasia.
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