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.


OBJECTIVE
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.
Anderson
K M
KM
Department of Medicine, The University of Illinois and the West Side VA Hospital, Chicago, IL, USA. kanderso@rush.edu
Bonomi
P
P
Hu
Y
Y
Harris
J E
JE
D000903:Antibiotics, Antineoplastic / Q000494:pharmacology; D017209:Apoptosis; D018929:Cell Culture Techniques / Q000379:methods; D002455:Cell Division; D045744:Cell Line, Tumor; D002470:Cell Survival; D003609:Dactinomycin / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D008962:Models, Theoretical; D009369:Neoplasms / Q000628:therapy; D002722:Chlorobenzenes
D000903:Antibiotics, Antineoplastic; D003609:Dactinomycin; D004791:Enzyme Inhibitors; D007211:Indoles; C060893:MK-886; D002722:Chlorobenzenes