calicheamicin-gamma(1)i and Leukemia--Promyelocytic--Acute

calicheamicin-gamma(1)i has been researched along with Leukemia--Promyelocytic--Acute* in 1 studies

Other Studies

1 other study(ies) available for calicheamicin-gamma(1)i and Leukemia--Promyelocytic--Acute

Article	Year
Modulation of nicotinamide adenine dinucleotide and poly(adenosine diphosphoribose) metabolism by calicheamicin gamma 1 in human HL-60 cells. Cancer letters, 1990, Apr-20, Volume: 50, Issue:2 The mechanism of calicheamicin gamma 1-mediated cytotoxicity was studied in human promyelocytic HL-60 leukemic cells. Calicheamicin gamma 1 caused an increase in poly(ADP-ribose) polymerase activity in HL-60 cells parallel to cell death. This effect of the drug correlated with a decrease in intracellular NAD+ level. 3-Aminobenzamide, an inhibitor of poly(ADP-ribosylation), prevented the calicheamicin gamma 1-triggered cytotoxicity in a dose-dependent manner. Simultaneous with the reversal of cytotoxicity, the addition of 3-aminobenzamide to drug-treated cells also inhibited the increase in poly(ADP-ribosylation) and the reduction in cellular NAD+ content. These results indicate that poly(ADP-ribosylation) activation and the subsequent perturbations in NAD(+)-dependent metabolic reactions are associated with the cytotoxic properties of the antitumor antibiotic calicheamicin gamma 1. Topics: Aminoglycosides; Anti-Bacterial Agents; Antibiotics, Antineoplastic; Benzamides; Cell Survival; DNA Damage; DNA, Neoplasm; Enediynes; Humans; Leukemia, Promyelocytic, Acute; NAD; Nucleoside Diphosphate Sugars; Poly Adenosine Diphosphate Ribose; Poly(ADP-ribose) Polymerase Inhibitors; Poly(ADP-ribose) Polymerases; Tumor Cells, Cultured	1990

Article

Year

Modulation of nicotinamide adenine dinucleotide and poly(adenosine diphosphoribose) metabolism by calicheamicin gamma 1 in human HL-60 cells.

Cancer letters, 1990, Apr-20, Volume: 50, Issue:2

The mechanism of calicheamicin gamma 1-mediated cytotoxicity was studied in human promyelocytic HL-60 leukemic cells. Calicheamicin gamma 1 caused an increase in poly(ADP-ribose) polymerase activity in HL-60 cells parallel to cell death. This effect of the drug correlated with a decrease in intracellular NAD+ level. 3-Aminobenzamide, an inhibitor of poly(ADP-ribosylation), prevented the calicheamicin gamma 1-triggered cytotoxicity in a dose-dependent manner. Simultaneous with the reversal of cytotoxicity, the addition of 3-aminobenzamide to drug-treated cells also inhibited the increase in poly(ADP-ribosylation) and the reduction in cellular NAD+ content. These results indicate that poly(ADP-ribosylation) activation and the subsequent perturbations in NAD(+)-dependent metabolic reactions are associated with the cytotoxic properties of the antitumor antibiotic calicheamicin gamma 1.

Topics: Aminoglycosides; Anti-Bacterial Agents; Antibiotics, Antineoplastic; Benzamides; Cell Survival; DNA Damage; DNA, Neoplasm; Enediynes; Humans; Leukemia, Promyelocytic, Acute; NAD; Nucleoside Diphosphate Sugars; Poly Adenosine Diphosphate Ribose; Poly(ADP-ribose) Polymerase Inhibitors; Poly(ADP-ribose) Polymerases; Tumor Cells, Cultured

1990