M. Potter – författare
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4 produkter
Häftad, Engelska, 1979
1 116 kr
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F. Melchers, M. Potter, NL. Warner HISTORICAL Prior to 1964 many workers had experienced considerable difficulty in establishing continuous lines of murine plasmacytoma in culture. Pettingill and Sorenson in 1966 grew X5563 after a painstaking period of adaptation. During a visit to the Salk Instiute in 1965 Leo Sachs began experiments with K. Horibata,E. S. Lennox and M. Cohn that ulti- mateley convinced most workers that murine plasmacytomas could be grown in vitro with ease. They adapted MOPC-21 * {called P3 at the Salk Institute) to in vitro culture and showed the cells produced a large amount of the IgG1 myeloma protein. Horibata, Lennox and Sachs did not report the important finding though a manuscript was written and accepted. The reason for the failure to publish the paper was that the original line was not recovered from the freezer and knowing there would be many requests for it the paper was withdrawn. As it later turned out, the failure to recover the line may have been triv- ial, for Horibata and Harris (1970) soon re-established a continuous line of P3 now named P3K. This line was distributed to other workers including Cesar Milstein in Cambridge.Soon after the success with P3, Scharff and colleagues at Albert Einstein established MPC-11*in cul- ture. Up to now continuous growth of human myeloma cells in vitro has remained a formidable problem.
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Sponsored by the National Cancer Institute (NIH)
E-bok
PDF, Engelska, 20121 459 kr
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Del 113 - Current Topics in Microbiology and Immunology
Oncogenes in B-Cell Neoplasia
Workshop at the National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, March 5–7, 1984
Häftad, Engelska, 2011
1 116 kr
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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.