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.
Department of Medicine, The University of Illinois and the West Side VA Hospital, Chicago, IL, USA. kanderso@rush.edu
K M
KM
Anderson
P
P
Bonomi
Y
Y
Hu
J E
JE
Harris
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