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Prevention of Programmed Cell Death in Burkitt Lymphoma Cell Lines by Bcl-2-dependent and -Independent Mechanisms by Anne E. Milner; Gerald D. Johnson; Christopher D. Gregory is a Medicine article available to read on EtoBox.

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## Abstract Burkitt lymphoma (BL) cell lines which retain the phenotypic characteristics of the freshly‐isolated tumour cells (group I cells) readily enter programmed cell death (apoptosis) in response to a variety of triggers. By contrast, isogenic BL cells which are phenotypically altered as a result of activation of their resident EBV genome (group‐III cells) are highly protected from apoptosis. Phenotypic changes in group‐III cells include the up‐regulation of the oncogene, __bcl__‐2. Expression of the 26‐kDa __bcl__‐2 protein in group‐1 BL cells following gene transfer was found to afford protection from apoptosis: the degree of protection was proportional to the amount of __bcl__‐2 protein expressed. When group‐1 __bcl__‐2 transfectants were compared with their group‐III counterparts it was found that, whilst __bcl__‐2 made a significant contribution in protecting from entry into apoptosis, hyper‐expression of __bcl__‐2 protein in group‐1 cells (well beyond that of group‐III cells) was necessary to attain the high levels of protection observed in group‐III cells. These results suggested that additional, __bcl__‐2‐independent, survival mechanisms could operate in BL cells. In

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Author

Anne E. Milner; Gerald D. Johnson; Christopher D. Gregory

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)

Published

1992

Language

EN

Field

Medicine (Health Sciences)