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Anderson, K.M. et al.

Anderson, Bonomi, Hu, Harris,

An interaction between type 1 and type 2 programmed cell death and clonogenic survival.

We suggest two additional reasons why current, non-surgical therapies for most solid, epithelial-derived cancers can lack effectiveness. Studies with panc-1 human pancreatic cancer cells cultured with actinomycin D and/or MK 886 indicate firstly, that type 2 (intrinsic, autophagic, mitochondrial-dependent, MK 886-induced) programmed cell death is less effective than the type 1 (apoptotic, extrinsic, ligand-dependent, actinomycin D-induced) form in reducing the number of residual clonogenic cells, and secondly, that activation of cellular suicide during their combined culture results in a greater number of residual clonogenic cells compared with either agent alone. HYPOTHESIS: Based on results from the culture of panc-1 cells with MK 886 and/or actinomycin D, we suggest that in this system, and possibly in others: (a) type 2 programmed cell death is a less effective inhibitor of residual cells with clonogenic potential, and (b) activation together of both forms of PCD increases the number of residual clonogenic cells.[1]

References

An interaction between type 1 and type 2 programmed cell death and clonogenic survival. Anderson, K.M., Bonomi, P., Hu, Y., Harris, J.E. Med. Hypotheses (2003) [Pubmed]

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