Overcoming resistance of XXXX cells to apoptosis.

@entity5 @entity588 @entity23996
Discovery of the B cell lymphoma gene 2 ( @entity588 gene) led to the concept that development of @entity5 required the simultaneous acquisition, not only of deregulated cell division, but also of resistance to programmed cell death or apoptosis. Apoptosis is arguably the common pathway to cell death resulting from a range of therapeutic initiatives, so that understanding the basis for the resistance of @entity5 cells to apoptosis may hold the key to development of new treatment initiatives. Much has already been learnt about the apoptotic pathways in @entity5 cells and proteins regulating these pathways. In most cells, apoptosis is dependent on the mitochondrial dependent pathway. This pathway is regulated by pro- and anti-apoptotic members of the @entity588 family, and manipulation of these proteins offers scope for a number of treatment initiatives. Effector caspases activated by the mitochondrial pathway or from death receptor signaling are under the control of the @entity23996 ( @entity23996 ) family. Certain proteins from mitochondrial can, however, competitively inhibit their binding to effector caspases. Information about the structure of these proteins has led to initiatives to develop therapeutic agents to block the @entity23996 family. In addition to development of selective agents based on these two ( @entity588 and @entity23996 ) protein families, much has been learnt about signal pathways that may regulate their activity. These in turn might provide additional approaches based on selective regulators of the signal pathways.
