Growth Arrest Specific Productivity and Apoptosis

Studies of p53 and c-mychave revealed a close relationship between cell proliferation and apoptosis. These studies may have important implications for process optimization strategies that have centered on the control of cellular proliferation. Such an approach allows for improvements in specific recombinant protein productivity during cultures that exhibit a negative correlation between growth rate and productivity. Furthermore, by controlling maximum cell number at an optimal level, cell death due to limitation of nutrients and oxygen should be minimized, thus simplifying medium clarification during downstream processing. However, such studies have had one major drawback: when attempts were made to control cellular proliferation, the cultures rapidly lost viability (93,94), and it would appear that, at least in the case of hybridoma cultures, this was due to the induction of apoptosis (85). Thus strategies designed to control cellular proliferation must also incorporate methods that minimize apoptosis. Initial results would appear to suggest that such an approach does work. Simpson et al. (8) found that Bcl-2 overexpression delays hybridoma cell death following cell cycle arrest induced by thymidine treatment. Similar results have been reported during Burkitt's lymphoma cultures (81).

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