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)

We have stored at -196 degrees C peripheral blood buffy coat (BC) and bone marrow (BM) cells collected from 47 patients with chronic granulocytic leukaemia in the chronic phase. Dimethyl sulphoxide (DMSO) 10% was used as cryoprotective agent. As these cells include CFUc and probably pluripotential stem cells they may be transfused as part of the management of patients who enter blast cell transformation. The mean numbers of nucleated cells collected and stored per procedure was about 9 times greater for BC collections than for BM harvests (106 +/- 49 (SD) X 10(9) versus 11.9 +/- 6.6 X 10(9) respectively). Agar CFUc assay showed that stored cells may remain viable for up to 5 years. Since in vitro studies showed that CFUc proliferation is not inhibited by low concentrations of DMSO the removal of all DMSO during cell reconstitution before transfusion may not be necessary. If autologous BC cells are capable of repopulating the BM of patients treated for CGL in blast cell transformation the routine collection and storage of BC rather than BM cells may be desirable for all newly diagnosed patients.
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PMID:Collection, cryopreservation and subsequent viability of haemopoietic stem cells intended for treatment of chronic granulocytic leukaemia in blast-cell transformation. 3 Apr 69

The Friend erythroleukemia cell line T3-C12, which produces Friend murine leukemia virus (F-MuLV) and can be induced to synthesize hemoglobin by dimethyl sulfoxide (DMSO), was monitored for viral RNA-dependent DNA polymerase reverse transcriptase (RT) activity. The amount of viral 60-70S RNA released from DMSO-treated cells was unaffected or increased compared to that from control cells, while RT activity from treated cells was decreased. Accordingly, the specific activity in F-MuLV from DMSO-treated cells expressed as RT/70S RNA was decreased to 8% of the control activity. The 5-bromo-2'-deoxyuridine added to cultures containing DMSO reversed the differentiation process, and the F-MuLV thus treated did not exhibit the reduced RT activity normally observed in DMSO-treated virus. Cell-free F-MuLV incubated with and without DMSO showed the same RT activity, indicating that DMSO itself did not inhibit RT activity. However, when F-MuLV-containing pellets from control and DMSO-treated culture fluids were mixed, there was marked inhibition of the control RT activity, suggesting that RNase hybrid activity was stimulated or that an inhibitor was produced. Assays of F-MuLV-RNase hybrid released from control and DMSO-treated cells showed no difference in activity, indicating that a specific inhibitor of RT was produced or activated. Additions of certain nucleotide triphosphates to RT incubation mixtures did not result in any stimulation of RT activity in DMSO-treated F-MuLV, suggesting that phosphatase was not responsible for the observed inhibition. The results suggested that DMSO treatment of T3-C12 cells caused a reduction in viral RT activity by stimulating the production of an inhibitor, the nature of which is unknown.
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PMID:Viral reverse transcriptase suppression associated with erythroid differentiation of Friend leukemia cells. 6 77

Low molecular weight chromatin peptides exert a dose-dependent inhibition of Dimethylsulfoxide (DMSO)-induced erythroid differentiation of murine Friend Leukemia Cells (FLC). This effect correlates with the degree of purification of the peptide fractions. Crot analysis of globin mRNA amounts in DMSO-treated FLC given the peptides showed a 4-5-fold decrease of messenger RNA in the cytoplasma with no nuclear storage of globin transcripts. Spectrin accumulation in "induced" FLC is inhibited as well. The effects of the peptides on erythroid markers are reversible upon removal of the compounds. They also appear to be specific for induced gene expression as (1) no effects are observed on cell growth and RNA synthesis in normal non-differentiating cell lines; and (2) no changes have been detected with regard to the expression of integrated viral genes coding for continuous shedding of viral particles.
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PMID:Effects of a chromatin low molecular weight peptidic fraction on differentiation markers and virus production in Friend leukemia cells. 9 93

Nicotinamide, a specific inhibitor of poly(ADP-ribose) synthetase, was found to be a moderate inducer of hemoglobin synthesis in Friend erythroid leukemia cells (FLC). Therefore, the effect of other inducers, s-ch as dimethyl sulfoxide (DMSO), hexamethylene-bisacetamide (HMBA), and butyrate, on poly(ADP-ribose) synthesis was examined. The extent of poly(ADP-ribose) synthesis in nuclei of FLC treated with DMSO or HMBA began to decrease before many phenotypic changes including hemoglobin production and reached 30--50% of the level of nontreated control when the cells enter the stationary phase. FLC variants unresponsive to HMBA or DMSO did not exhibit as low an activity of poly(ADP-ribose) synthesis as their parent cells did by treatment with these inducers. In contrast, butyrate stimulated poly(ADP-ribose) synthesis transiently but distinctly (about 50%) at an early stage of culture (6--24 hr), but suppressed it at a later stage. Neither the cell growth nor degradation of poly(ADP-ribose) is correlated with the effect of inducers. These results suggest that the level of poly(ADP-ribose) synthesis is correlated with the differentiation of FLC.
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PMID:Erythroid differentiation and poly(ADP-ribose) synthesis in Friend leukemia cells. 15 37

The effect of mouse interferon (ITF) on the expression of Friend leukaemia virus (FLV) an on dimethyl sulphoxide (DMSO)-stimulated haemoglobin synthesis in Friend erythroleukaemic cells (FLC) was studied. Immunofluorescent staining was used to detect intracellular antigens, and incorporation of 3H-uridine into virions to detect extracellular virus release. Interferon markedly inhibited haemoglobin synthesis and FLV production, but enhanced accumulation of virus antigens in the cytoplasm; on the cell surface, however, FLV antigens were present to the same extent whether ITF was present or not. When ITF was removed, virus production rose and intracellular virus antigens fell to the levels of untreated controls.
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PMID:Production of Friend leukaemia antigens in chronically-infected cells treated with interferon. 56 23

The factors that control oncornavirus formation were analyzed in Friend leukemia cells that undergo hematopoiesis when treated with dimethyl sulfoxide. Suspension cultures of Ostertag FSD-1 cell line were found to enter a G or resting state at the end of their proliferative phase and to simultaneously cease producing helper and dependent components of Friend virus. Whereas the decline in virus production is at least 100-fold, rates of cellular RNA and protein synthesis are only slightly lower in resting than in growing cells. Both resting and growing cells contain similarly large concentrations of the viral proteins P(30) and P(12). Dimethyl sulfoxide induces hemoglobin synthesis in growing cells, but its effects on virus production appear to be indirect results of its action to inhibit cell growth and thus to delay entry of cells into the G resting state. Furthermore, variant cell lines were obtained with differing abilities to synthesize virus or hemoglobin. Some lines no longer produce infectious virus, although they all harbor murine leukemia virus genes which are expressed to varying extents. The major internal protein of these oncornaviruses, P(30), is synthesized in large amounts by all of the cell lines. These results suggest that Friend virus production is not coinduced with erythroid differentiation, as had been proposed, but rather is controlled by a cellular growth cycle.
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PMID:Relationship of Friend murine leukemia virus production to growth and hemoglobin synthesis in cultured erythroleukemia cells. 106 78

We have reported that dimethyl sulfoxide (DMSO) and antineoplastic agents exhibit synergistic cytotoxicity against human tumors in vitro. This study was undertaken to investigate this effect in vivo. Groups of mice were given intraperitoneal (i.p.) injections of P388 leukemia cells. Groups were treated with i.p. injections of either saline, DMSO alone, mitoxantrone hydrochloride (DHAD) alone, methotrexate alone, DHAD in DMSO or methotrexate in DMSO. Combinations of DMSO and DHAD produced 46-61% increases above expected survival, demonstrating synergistic cytotoxicity in vivo. Following confirmatory animal studies, trials utilizing i.p. delivery of antineoplastics in DMSO as treatment for peritoneal tumors should be undertaken.
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PMID:Synergistic cytotoxicity of combinations of dimethyl sulfoxide and antineoplastic agents against P388 leukemia in CD-F1 mice. 128 34

A new nitroxyl labeled tetracycline is synthesized. Proton NMR experiments of tetracycline, spin-labeled tetracycline, and the diamagnetic reduced form in DMSO-d6 are reported. The signals observed in the NMR spectra are all assigned. The NMR data revealed that the spin label is attached to the C-2 amide group on ring A of tetracycline. The spin-labeled tetracycline is also tested in vitro for antitumor activity and is found to be active against leukemia P338/ADR cell line and in melanoma LOX cell line.
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PMID:Spectroscopic and biological studies of spin-labeled tetracycline. 131 98

The export of leukotriene (LT) C4 from human eosinophils, a carrier-mediated process that is temperature-dependent and saturable, was characterized further in eosinophils and in two human leukemia cell lines that do not present an intact 5-lipoxygenase pathway. In eosinophils, KG-1 cells, and dimethyl sulfoxide (DMSO)-differentiated HL-60 cells, the respective Q10 values for temperature-dependent LTC4 export were 3.7, 3.3, and 3.4 and for energy of activation were 28.2 kcal/mol, 23.0 kcal/mol, and 27.8 kcal/mol (1 kcal = 4.18 kJ). When human eosinophils, KG-1 cells, and DMSO-differentiated HL-60 cells were preloaded with defined amounts of intracellular LTC4 by incubation with LTA4 and with incremental amounts of a glutathione conjugate, S-dinitrophenyl glutathione (GS-DNP) by sequential incubation with 1-chloro-2,4-dinitrobenzene, GS-DNP inhibited the export of LTC4 in a dose-dependent manner. By plotting the ratio of total GS-DNP (cell retained plus released) to the sum of total GS-DNP plus total LTC4 against the percentage inhibition of LTC4 release, IC40 values of 0.839, 0.803, and 0.841 were obtained for eosinophils, KG-1 cells, and DMSO-differentiated HL-60 cells, respectively. When cells preloaded with LTC4 were resuspended in incremental concentrations of the organic acid transport inhibitor, probenecid, there was a dose-dependent decrease in LTC4 release; GS-DNP and probenecid inhibited LTC4 release in a cumulative fashion, whereas neither inhibited the release of LTB4 from preloaded nondifferentiated HL-60 cells. Therefore, LTC4 export from cells of bone marrow origin occurs through a probenecid-sensitive membrane carrier shared by other glutathione conjugates and distinct from the LTB4 carrier export system.
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PMID:Leukotriene C4 uses a probenecid-sensitive export carrier that does not recognize leukotriene B4. 133 13

We and others have previously shown that microtubules (MT) are stained more intensely and are organized differently in differentiating leukemia cells. To study the effects of the MT disrupting drugs, colchicine (Coln) and vincristine (VCR), on the maturation process, HL-60 leukemia cells were pretreated with Coln or VCR for 1 h and then exposed to either retinoic acid (RA) or dimethyl sulfoxide (DMSO). Neither Coln nor VCR induced the differentiation of HL-60 cells, but in combination with RA increased the percentage of nitroblue tetrazolium-positive cells, the expression of the mature myelocyte surface marker Mo 1, and the content of MT over the effects produced by RA alone. In contrast, pretreatment with Coln or VCR delayed the commitment to a differentiation pathway induced by DMSO. The supra-additivity exhibited between Coln and RA required the administration of Coln prior to RA; thus, Coln had no effect when given two days after the cellular exposure to RA. The findings suggest that (a) a combination of non-cytotoxic concentrations of Coln or VCR with RA may have clinical utility as inducers of leukemia cell maturation, and (b) MT may be involved in modulating signal transduction during the initiation of HL-60 cell differentiation.
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PMID:The effects of microtubule disrupting drugs on the differentiation of HL-60 leukemia cells. 140 22


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