Treatment of human clonogenic tumor cells and bone marrow progenitor cells with bleomycin and peplomycin under 40.5°C hyperthermia in vitro

1989 ◽  
Vol 25 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Herbert A. Neumann ◽  
Dieter B. Herrmann ◽  
Heinz H. Fiebig ◽  
Rupert Engelhardt
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Tumor Cells ◽  
Bone Marrow Progenitor Cells ◽  
Bone Marrow Progenitor ◽  
Clonogenic Tumor Cells

scholarly journals 2'-Deoxycytidine protects normal human bone marrow progenitor cells in vitro against the cytotoxicity of 3'-azido-3'-deoxythymidine with preservation of antiretroviral activity

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 1923-1928 ◽  
Author(s):  
K Bhalla ◽  
M Birkhofer ◽  
GR Li ◽  
S Grant ◽  
W MacLaughlin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
High Dose ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Bone Marrow Progenitor Cells ◽  
Bone Marrow Progenitor ◽  
High Concentrations ◽  
Anti Hiv

Abstract Bone marrow cytotoxicity of 3′-azido-3′-deoxythymidine (AZT), an anti- human immunodeficiency virus (anti-HIV) drug, has been attributed to deoxyribonucleotide pool perturbations that might result in impaired DNA synthesis in normal bone marrow elements. We examined, in vitro, the effect of high, but clinically achievable and nontoxic, concentrations of 2′-deoxycytidine (dCyd) (greater than or equal to 100 mumol/L) on high-dose AZT mediated growth inhibition and intracellular biochemical perturbations in normal bone marrow progenitor cells. Colony formation by bone marrow progenitor cells in semisolid medium was significantly protected by dCyd against the inhibitory effects of co-administered, high concentrations of AZT (10 mumol/L). Also, dCyd significantly corrected AZT mediated depletion of intracellular thymidine triphosphate (dTTP) and dCyd triphosphate (dCTP) levels in normal bone marrow mononuclear cells (BMMC). Moreover, dCyd reduced the intracellular accumulation of AZT triphosphate (AZT-TP) and its DNA incorporation in BMMC. In contrast, co-administration of dCyd (100 mumol/L to 1 mmol/L) did not reverse AZT (10 mumol/L) mediated suppression of HIV infectivity in HUT-102 cells in culture, although a partial reduction in intracellular AZT-TP pools and its DNA incorporation as well as a correction of AZT mediated depletion of dTTP and dCTP pools was observed in these cells. These studies suggest that dCyd at high concentrations might ameliorate the bone marrow cytotoxicity of high-dose AZT without impairing its anti-HIV effect.

Epidemiology: Culture of bovine bone marrow progenitor cells in vitro

2001 ◽  
Vol 23 (4) ◽  
pp. 170-175 ◽  
Author(s):  
V. Van Merris ◽  
M. Lenjou ◽  
D. Hoeben ◽  
G. Nijs ◽  
D. Van Bockstaele ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Bovine Bone ◽  
Bone Marrow Progenitor Cells ◽  
Bone Marrow Progenitor

scholarly journals 2'-Deoxycytidine protects normal human bone marrow progenitor cells in vitro against the cytotoxicity of 3'-azido-3'-deoxythymidine with preservation of antiretroviral activity

Blood ◽  
1989 ◽  
Vol 74 (6) ◽  
pp. 1923-1928
Author(s):  
K Bhalla ◽  
M Birkhofer ◽  
GR Li ◽  
S Grant ◽  
W MacLaughlin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
High Dose ◽  
Normal Bone Marrow ◽  
Normal Bone ◽  
Bone Marrow Progenitor Cells ◽  
Bone Marrow Progenitor ◽  
High Concentrations ◽  
Anti Hiv

Bone marrow cytotoxicity of 3′-azido-3′-deoxythymidine (AZT), an anti- human immunodeficiency virus (anti-HIV) drug, has been attributed to deoxyribonucleotide pool perturbations that might result in impaired DNA synthesis in normal bone marrow elements. We examined, in vitro, the effect of high, but clinically achievable and nontoxic, concentrations of 2′-deoxycytidine (dCyd) (greater than or equal to 100 mumol/L) on high-dose AZT mediated growth inhibition and intracellular biochemical perturbations in normal bone marrow progenitor cells. Colony formation by bone marrow progenitor cells in semisolid medium was significantly protected by dCyd against the inhibitory effects of co-administered, high concentrations of AZT (10 mumol/L). Also, dCyd significantly corrected AZT mediated depletion of intracellular thymidine triphosphate (dTTP) and dCyd triphosphate (dCTP) levels in normal bone marrow mononuclear cells (BMMC). Moreover, dCyd reduced the intracellular accumulation of AZT triphosphate (AZT-TP) and its DNA incorporation in BMMC. In contrast, co-administration of dCyd (100 mumol/L to 1 mmol/L) did not reverse AZT (10 mumol/L) mediated suppression of HIV infectivity in HUT-102 cells in culture, although a partial reduction in intracellular AZT-TP pools and its DNA incorporation as well as a correction of AZT mediated depletion of dTTP and dCTP pools was observed in these cells. These studies suggest that dCyd at high concentrations might ameliorate the bone marrow cytotoxicity of high-dose AZT without impairing its anti-HIV effect.

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