Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism of 14C-lysine by leukaemic cells in acute myeloblastic, myelomonocytic, lymphoblastic and chronic myeloid leukaemia with blast crisis was studied. The investigations included lysine metabolism to CO2, lipids, organic acids and nucleotides and its incorporation into cellular proteins. The obtained results were compared with determinations carried out in granulocytes and lymphocytes of healthy subjects. Cells in acute leukaemias metabolized 14C-lysine in a similar range. In relation to normal cells the range of lysine metabolism to lipids in the leukaemic cells was significantly higher (p less than 0.01), while that of organic acids was significantly lower (p less than 0.05). The activity of 14C-lysine metabolism depended on the number of blast cells in the sample and the type of acute leukaemia. Neoplastic cells in blast crisis and in acute myeloblastic leukaemia incorporated more actively 14C-lysine into proteins than cells in acute myelomonocytic and acute lymphoblastic leukaemia (p less than 0.05). Similar differences in lysine metabolism were observed between myelomonocytes and blast cells from acute lymphoblastic leukaemia (p less than 0.05).
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PMID:[Lysine metabolism in acute leukemia]. 29 72

L1210 murine leukemia cells grow in an ascites plasma that contains lipids, including 0.62 +/- 0.046 (S.E.) MICRONEq free fatty acid per ml. in vitro incubations demonstrated that isolated L1210 cells readily utilize free fatty acid that is added to the incubation medium. When the cells were incubated with albumin-bound [1-14C]palmitate, about 12 times more radioactivity was incorporated into cell lipids than was oxidized to CO2. Triacylglycerols contained 1.5 to 4 times more radioactivity than phospholipids, and from 48 to 69% of the phospholipid radioactivity was recovered in the choline phosphoglycerides. [1-14C]Palmitate utilization increased as the fatty acid concentration of the medium was raised, the largest increase occurring in the triacylglycerol fraction. Palmitate utilization also was increased by the presence of carbohydrates in the medium, their effectiveness (in descending order) being glucose, mannose, galactose, fructose, and glycerol. By contrast, ribose did not produce any stimulatory effect. During a 1-hr incubation, between 82 and 87% of the [1-14C]palmitate that was taken up remained as palmitic acid. From 8 to 15% was elongated to stearate, and only 2 to 3% was desaturated to palmitoleate and oleate. Based upon the lipid content, growth rate, and palmitate utilization rate of the cells, it appears that a major portion of the lipid requirements of the L1210 cell may be supplied by the fatty acid contained in the ascites plasma. In addition, our results suggest that most of the saturated fatty acid taken up is incorporated into cell lipids without structural modification.
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PMID:Fatty acid utilization by L1210 murine leukemia cells. 55 21

P388 (murine) and CEM (human) leukemia cells were exposed in vitro to a serine-deprived medium. Cultivation was carried out at 37 degrees C, 5% CO2. Proliferation assay was conducted with a RPMI 1640 medium (control) and a serine-deprived medium for 3 days. The deprivation of serine reduced the proliferation of both cells, and the necessity of serine for the cell proliferation was thus recognized. The effects of the substance on the level and pattern of intracellular amino acids were observed. P388 cells exposed to serine-deprived medium for 3 h were then transferred to the control medium. The cellular amino acid levels were determined at the time of medium change and 1, 2, 3 h thereafter. Serine-deprivation improved intracellular amino acids in comparison with those from control, and the medium change to control reduced their levels. Therefore, extracellular serine appeared to regulate the efflux of amino acids from cells. This suggests that serine-deprivation may be useful for anticancer drug retention in the cells.
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PMID:Stimulation of amino acid efflux from cells by extracellular serine. 134 49

Triptolide (Tri) is a diterpenoid triepoxide isolated from Tripterygium wilfordii Hook F. The effects of Tri on the colony formation of breast cancer cell lines MCF-7 and BT-20, stomach cancer cell lines MKN-45, MKN-7, and KATO-III, and promyelocytic leukemia cell line HL-60 were reported. Using Hamburger-Salmon's double layer agar technique with certain modifications, cancer cells were cultured in 0.3% agar in a highly humidified atmosphere of 5% CO2 at 37 degrees C for 14-21 d. Colonies were counted on d 14 (occasionally d 21) with the colony analyzer system CA-7A. Of the 5 solid tumor cell lines tested, 4 showed diminished colony formation in soft agar by greater than 70% of control value in Tri 10(-8) mol.L-1 (continuous exposure). The magnitudes of the inhibitory effect of Tri on most breast and stomach cancer cell lines were similar to that on the leukemia cell line HL-60. IC50 were 0.504-1.22 micrograms.L-1. The clinically achievable peak plasma concentration (PPC) of Tri was estimated as 0.15 mg.L-1, being 72-126 times higher than the IC70 of the cancer cell lines except KATO-III. The results suggest that Tri might have a potential therapeutic effect on some types of solid tumors, e.g., breast and stomach cancers.
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PMID:Inhibitory effect of triptolide on colony formation of breast and stomach cancer cell lines. 181 94

The PO2 measured in a sample of blood can be misleadingly low, owing to consumption of oxygen in vitro in patients with leukemia. The purpose of this study was to determine whether a rise in PCO2 in such blood could be a useful indication of consumption of oxygen in vitro. Because of the non-bocarbonate buffer capacity of blood and the carriage of CO2, mainly as bicarbonate, we reasoned that the rise in PCO2 would be too small to be helpful. Hence the quantitative relationship between the consumption of oxygen and the production of CO2 in blood was determined. Other reactions yielding CO2 (the titration of lactic acid) were monitored. Consumption of oxygen was stimulated in blood of normals in vitro by adding methylene blue (100 mumol/L); in addition, blood from four patients with leukemia was studied without additions. The rate of consumption of oxygen at 22 degrees C was linear over 60 min; the respiratory quotient was close to unity. The rise in PCO2 was small even when the fall in PO2 was 60 mmHg. We conclude that a rise in PCO2 is not a reliable way to diagnose consumption of oxygen in blood in vitro as patients may hyperventilate, making it very difficult to recognize a small rise in PCO2.
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PMID:Can oxygen consumption in blood in vitro be detected by a change in PCO2? 190 1

A eukaryotic growth medium (Program Development Research Group Basal Growth Medium) was developed for CO2-independent maintenance and propagation of human and nonhuman tumor cell lines representing diverse histologies (e.g., cancers of the brain, colon, lung, ovary, and kidney, as well as leukemia and melanoma). It was also shown to be suitable for the maintenance and propagation of nontumor cells of human and nonhuman derivation. The medium derives its buffering capacity primarily from beta-glycerophosphate, exhibits a stable physiologic pH of 7.3-7.4, and is optimized to facilitate growth in atmospheric CO2. It is also useful in cellular growth and cytotoxicity assays based on either the metabolic reduction of tetrazolium reagents or protein staining. The 50% inhibitory concentration values obtained with carmustine, doxorubicin, and tamoxifen in cell lines maintained in the new medium under atmospheric CO2 were closely comparable to those obtained with these drugs against cells maintained in RPMI-1640 under a 5% CO2 environment.
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PMID:New carbon dioxide-independent basal growth medium for culture of diverse tumor and nontumor cells of human and nonhuman origin. 211

NaHCO3 activated the folylpolyglutamate synthetase (FPGS) from rat liver and the human leukemia cell lines K562 and CCRF-CEM by 1.7- to 2.0-fold. Optimal activation was achieved by 10 mM NaHCO3 in all cases; NaCl, sodium formate, sodium acetate, NaN3, and Na2SO3 at 10 mM did not cause activation. Activation could be masked if assay solutions which had extensively absorbed atmospheric CO2 were used. Activation of the human CCRF-CEM FPGS was examined in detail. Km and Vmax values for pteroyl substrates (aminopterin or methotrexate) and L-glutamate increased proportionally in the presence of NaHCO3; there was thus no apparent change in the catalytic efficiency (Vmax/Km) of the FPGS reaction with these substrates. However, NaHCO3 increased the efficiency of the reaction with respect to ATP by decreasing its apparent Km while increasing the Vmax of the reaction. NaHCO3 also activated FPGS activity when folic acid, dihydrofolic acid and tetrahydrofolic acid were substrates. The relative distribution of products synthesized from methotrexate or tetrahydrofolate by FPGS was not altered by addition of NaHCO3. The potency of 5,8-dideazapteroylornithine, an FPGS-specific inhibitor, was not changed by the presence of NaHCO3 (IC50 = 0.4 microM). These results suggest that FPGS activity with folates and classical antifolates may be activated at physiological concentrations of NaHCO3. In addition, inadvertent contamination of assay solutions with bicarbonate from atmospheric CO2 may cause artifacts in the determination of activity levels and kinetic constants of FPGS.
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PMID:Activation of mammalian folylpolyglutamate synthetase by sodium bicarbonate. 216 55

Syntheses and structure-activity relationships of 7-O-(3-amino-2,3,6-trideoxy-a-L-lyxo- (18), -L-arabino- (20) and -L-ribo- hexopyranosyl)-epsilon-isorhodomycins (25) and their 3'-dimethylamino derivatives 22, 23 and 26 are described. Condensation (trimethylsilyl triflate, molecular sieves 4 A, 10:1 dichloromethane-acetone, -15 degrees) of epsilon-isorhodomycinone (epsilon-isoRMN, 6) with 1,5-anhydro-4-O-p-nitrobenzoyl-3-trifluoroacetamido-L-lyxo- (5) -L-arabino- (9) or -L-ribo-hex-l-enitols (10) afforded mainly the 7-O-a-glycosyl-epsilon-isoRMNs 7, 11, and 12. Similar glycosylation of 6 with 1,5-anhydro-3-azido-4-O-p-nitrobenzoyl-2,3,6-trideoxy-L-arabino-hex-1-++ +enitol (15) yielded a-glycoside 16. Removal (M NaOH) of the p-nitrobenzoyl and trifluoroacetyl groups from 7, 11, and 12 gave the 7-O-(3-amino-2,3,6-trideoxy-a-L-hexopyranosyl)-epsilon-isoRMNs 18, 20, and 25. Reductive alkylation (CH2O, NaCNBH3) of these products afforded the 3'-N,N-dimethyl analogues 22, 23, and 26. The cytotoxic effect (IC50) of the semisynthetic epsilon-isorhodomycins was tested in vitro in leukemia cell line L1210.
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PMID:Semisynthetic epsilon-isorhodomycins: their synthesis using glycals and their structure-activity relationship. 222 81

In order to investigate the incidence of pulmonary function complications following bone marrow transplantation (BMT), 17 patients with leukaemia and 8 with aplastic anaemia were sequentially assessed over a one year period. Before BMT, all the patients were free of respiratory symptoms and had both normal chest X-ray and routine lung function tests. However, 5 patients disclosed airway hyperreactivity. Aplastic anaemia patients had significantly lower haemoglobin-adjusted diffusing capacity for carbon monoxide (DLCO) than those with leukaemia, a finding significantly related to the lower haemoglobin values shown in the former individuals. Following BMT there were transient mild to moderate reductions in DLCO and static lung volumes; moreover, patients with leukaemia had lower DLCO than those with aplastic anaemia. Fourteen of the 25 patients had ventilatory defects, including 10 individuals with bronchial hyperresponsiveness. Post-BMT lung function changes were transiently accompanied by mild to moderate symptoms of respiratory disease in most of the patients.
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PMID:Lung function in allogeneic bone marrow transplantation recipients. 266 Dec 59

Little is known of pulmonary function in survivors of acute lymphoblastic leukaemia (A.L.L.); this is despite the fact that some drugs used, most notably methotrexate, have well-recorded pulmonary toxicity, and the most common infections during therapy in most series are of upper and lower respiratory tract. As part of a survey of all cancer survivors attending the Royal Hospital for Sick Children in Edinburgh, 38 leukaemic patients, who had completed treatment 3 months to 14 years 6 months (median 6 years and 8 months) prior to survey were assessed with regards to their respiratory status. Each patient completed a questionnaire and had spirometry and lung volumes measured; 30 patients additionally had transfer factor for carbon monoxide (TCO) measured. There were 21 children, 11 adults, and 6 patients in the age range between child and adult. Of the 26 adults and children studied with complete data available, 17 (65%) had one or more low values for vital capacity (VC), total lung capacity (TLC), residual volume, or TCO. Mean VC, TLC and TCO were significantly lower than the mean of the predicted values (P less than .001). Gas transfer per unit lung volume (KCO) was normal in all cases. Few patients had symptoms of respiratory disease. There was an increased incidence of low TCO in patients diagnosed under 8 years of age. Impairment of lung growth could be a contributing factor to the observed abnormalities in pulmonary function. Impairment of pulmonary function in survivors of A.L.L. may be of significance for them in later life.
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PMID:Pulmonary function in childhood leukaemia survivors. 270 34


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