Share
oncogenes in b-cell neoplasia: workshop at the national cancer institute, national institutes of health, bethesda, md, usa, march 5 7, 1984
F. Melchers
(Illustrated by)
·
M. Potter
(Illustrated by)
·
M. Weigert
(Illustrated by)
·
Springer
· Paperback
oncogenes in b-cell neoplasia: workshop at the national cancer institute, national institutes of health, bethesda, md, usa, march 5 7, 1984 - Potter, M. ; Melchers, F. ; Weigert, M.
Choose the list to add your product or create one New List
✓ Product added successfully to the Wishlist.
Go to My Wishlists
Origin: U.S.A.
(Import costs included in the price)
It will be shipped from our warehouse between
Thursday, May 23 and
Monday, June 10.
You will receive it anywhere in United Kingdom between 1 and 3 business days after shipment.
Synopsis "oncogenes in b-cell neoplasia: workshop at the national cancer institute, national institutes of health, bethesda, md, usa, march 5 7, 1984"
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.
