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

Particulate membrane preparations from K-562 [human CML (chronic-myelogenous-leukaemia)-derived] cells catalyse the transfer of [3H]galactose from UDP-[3H]-galactose and [3H]N-acetylglucosamine from UDP-[3H]N-acetylglucosamine into an endogenous product that on digestion with Pronase yields long-chain glycopeptides (mol.wt. 7000--10 000) called 'erythroglycan'. Incorporation of either labelled sugar increased up to 60 min of incubation time. The labelled erythroglycan was isolated by chromatography on Sephadex G-50 and characterized by digestion with endo-beta-galactosidase from Escherichia freundii, followed by analysis on Bio-Gel P-2 and paper chromatography. This digestion gave the following four products: (1) a disaccharide with the sequence beta GlcNAc-beta Gal; (2) a trisaccharide with the sequence betaGal-betaGlcNAc-beta Gal; (3) a larger oligosaccharide containing galactose and N-acetylglucosamine; and (4) a putative protein-linkage region.
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PMID:Cell-free biosynthesis of erythroglycan in a microsomal fraction from K-562 cells. 679 62

Changes in sialoglycoconjugates and glycosphingolipid (GSL)5 metabolism were demonstrated in mouse EL4, P52 and YAC-1 lymphoma and L1210 leukemia cell lines treated with beta-interferon (IFN). Expression of cell surface (neuraminidase-releasable) sialic acid on IFN-treated cells was markedly elevated (three- to six-fold). The increase in neuraminidase-releasable sialic acid is contributed by sialoglycoproteins and particularly by cell-surface gangliosides in IFN-treated cells. Incorporation of [3H]-galactose into all GSL was elevated in IFN-treated cells. Thin-layer chromatographic analysis of GSL of IFN-treated cells showed an increase in several GSL homologues with striking changes in ganglioside with chromatographic migration of GM2, GM1, and GD1a relative to control cells. IFN-treated tumor-cell lines became resistant to lysis by virus-induced IFN-activated natural killer (NK) cells, as shown previously, but addition of neuraminidase to IFN-treated and untreated cells caused only a moderate increase in NK-sensitivity. This suggests that IFN-mediated protection of target cells from NK lysis was not due to a preferential masking of target structure by elevated levels of sialic acid. These membrane-associated changes in GSL and sialic acid in IFN-treated cells may be potentially significant, because a correlation between certain GSL expression, sialic acid phenotype and susceptibility of target cells to NK-cell-mediated lysis have been found in several other systems.
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PMID:Interferon-induced increase in neuraminidase-releasable sialic acid and glycosphingolipid metabolism in mouse lymphoma and L1210 leukemic cell lines: correlation with susceptibility to natural killer cell-mediated lysis. 683 56

In L1210 leukemia cells, 6-deoxy-6-fluoro-D-galactose specifically inhibited the incorporation of [3H]-D-galactose, while that of other precursors of glycoconjugate biosynthesis, including mannose and glucosamine, was unaffected. The activation of [6-3H]-6-deoxy-6-fluoro-D-galactose to a nucleotide sugar was similar to that found for [3H]-D-galactose. The incorporation of either sugar after 1 hr was visualized by electron microscopic autoradiography to be in the Golgi region. Treatment of L1210 cells with 6-deoxy-6-fluoro-D-galactose in vitro or in vivo resulted in a specific, dose- and time-dependent decrease in the activity of cell surface sialyltransferase (ectosialyltransferase) but not of 5'-nucleotidase, a plasma membrane marker enzyme. The decrease in ectosialyltransferase activity appeared to be selective and is suggested to be due to structural modification of the cell surface galactoprotein acceptors for this enzyme. The data indicate that 6-deoxy-6-fluoro-D-galactose is an effective modifier of cellular glycoconjugate in that its incorporation into certain cell surface components results in a modification of plasma membrane structure and function.
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PMID:Effects of a membrane sugar analogue, 6-deoxy-6-fluoro-D-galactose, on the L1210 leukemic cell ectosialyltransferase system. 684 4

A patient with coexistent Gaucher disease and Philadelphia positive chronic granulocytic leukemia (CGL), who subsequently developed myeloblastic leukemia, is described. The diagnosis of CGL was established according to standard clinical, morphological, biochemical, and cytogenetic data, while the diagnosis of true Gaucher disease was based on biochemical data and the presence of Gaucher cells with typical ultrastructural features in the bone marrow and spleen. Enzyme studies showed low activity of ceramide-beta-glucosidase in the patient's peripheral blood leukocytes, skin fibroblasts, and splenic tissue and the presence of increased amounts of ceramide-beta-glucoside in the spleen. This case is reported in order to draw attention to the possible coexistence of these two diseases in the same patient, as opposed to the well-recognized finding of "Gaucher-like" cells in the bone marrow of patients with CGL. Enzyme studies enable distinction between these two situations.
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PMID:Coexistence of Gaucher Disease and Philadelphia positive chronic granulocytic leukemia. 695 8

The presence of lymphocyte receptors for peanut agglutinin in significant numbers (greater than 15%) was identified on leukemic cells from T-cell acute lymphoblastic leukemia (T-ALL) (3/4), B-cell ALL (B-ALL) (2/4), null cell ALL (8/17), and on normal fetal thymic lymphocytes but not on normal human peripheral blood lymphocytes. Peanut agglutinin (PNA) binding was blocked specifically on leukemia lymphoblasts and thymic lymphocytes by the addition of galactose to the medium. When all immunologic subgroups of ALL are combined, preliminary data suggest that of the 13 ALL patients having greater than 15% PNA-positive lymphoblasts, 8 had relapsed, whereas none of the 12 ALL patients with less than 15% PNA-positive cells have recurrent disease at this time. It is likely that analysis of PNA receptors on ALL lymphoblasts may be a useful adjunct to the existing clinical and immunologic prognostic indicators.
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PMID:Receptors for peanut agglutinin (Arachus hypogea) in childhood acute lymphoblastic leukemia: possible clinical significance. 696 48

Acidic isoferritins have been identified as leukemia-associated inhibitory activity (LIA), which suppresses colony and cluster formation of colony-forming unit-granulocyte macrophages from normal donors but not from patients with leukemia. LIA was detected in all ferritin preparations tested, including ferritin isolated from normal heart, spleen, liver, and placental tissues, and from the spleens of patients with chronic myelogenous leukemia and Hodgkin's disease. Purified preparations of LIA were composed almost entirely of acidic isoferritins, as determined by immunoassay, radioimmunoassay, and isoelectric focusing. The inhibitory activity in the LIA and ferritin samples was inactivated by a battery of antisera specific for ferritin, including those prepared against acidic isoferritins from normal heart and spleen tissues from patients with Hodgkin's disease, and those previously absorbed with basic isoferritins. Antisera absorbed with acidic isoferritins did not inactivate the inhibitory activity. Separation of LIA and chronic myelogenous leukemia and normal spleen ferritin by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and isoelectric focusing confirmed that the regions of peak inhibitory activity corresponded in each to an apparent molecular weight of approximately 550,000 and to a pI value of 4.7. Similar physicochemical characteristics included inactivation by methods that dissociate ferritin molecules into subunits and by treatment with trypsin, chymotrypsin, pronase, and periodate. The purified preparations were extremely stable to heat treatment. The glycoprotein nature of the inhibitory activity was substantiated because it bound to concanavalin A-Sepharose and was eluted off by alpha-methyl mannose. Inhibitory activity of the activity of the acidic isoferritins was detected at concentrations as low as 10(-17)-10(-19) M and iron saturation did not appear to be necessary for its action. These results implicate acidic isoferritins in the regulation of normal myelopoiesis and suggest a role for them in the progression of leukemia.
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PMID:Identification of leukemia-associated inhibitory activity as acidic isoferritins. A regulatory role for acidic isoferritins in the production of granulocytes and macrophages. 697 99

The sugar composition of the surface glycoprotein from Friend murine leukemia virus was determined by gas-liquid chromatography of the alditol acetates and by the thiobarbituric acid method, respectively. N-Acetylglucosamine, mannose, galactose, sialic acid and fucose were found in a molar ratio around 15.2:11.6:7.4:3.3:1.0. Ten oligosaccharide fractions were obtained from glycoprotein preparations by a suitable sequence of degradation (with pronase, endo-beta-N-acetylglucosaminidase H, neuraminidase, and by hydrazinolysis) and separation procedures (concanavalin A-affinity chromatography and gel filtration). The qualitative sugar composition of these fractions was analyzed by in vivo labelling with D-[6-(3)H]glucosamine, D-[2-(3)H]mannose, D-[6-(3)H]galactose, or L-[6-(3)H]fucose, and their molecular weights were estimated from the gel elution volumina. Four fractions of N-glycosidically linked oligosaccharides of the oligomannosidic ('high mannose') type oligomannosidic7-oligomannosidic10, about seven to ten sugar residues), two of the mixed (M11 and M12), and four of the N-acetyllactosaminic ('complex') type (N-acetyllactosaminic9, probably nine sugar residues; N-acetyllactosaminica-N-acetyllactosaminic c, size unknown) were thus identified.
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PMID:Separation procedure and sugar composition of oligosaccharides in the surface glycoprotein of Friend murine leukemia virus. 712 44

We have isolated a mutant Rauscher murine leukemia virus (R-MuLV) with a mutation in its envelope (env) glycoprotein gene. This mutant encodes a membrane glycoprotein with an apparent Mr = 80,000 (gPr80env) that contains both gp70 and p15E antigenic determinants found in the larger wild type R-MuLV env precursor molecule gPr90env. Glycosylation inhibition and peptide mapping analyses indicate that the smaller size of the mutant glycoprotein is caused by a shortening of its polypeptide chain rather than by reduced glycosylation. Unlike gPr90env of wild type R-MuLV which contains Asn-linked high mannose oligosaccharides and is processed by partial proteolysis and by further glycosylation in the Golgi apparatus to produce gp70 plus p15E, the mutant glycoprotein can reach the cell surface without proteolysis. The uncleaved plasma membrane component, which undergoes further glycosylation during its transit through the Golgi apparatus, has an apparent Mr = 85,000. Furthermore, this cell surface glycoprotein is incorporated into released virions which are infectious. However, the mutant envelope glycoproteins on the cell surface do not block the receptors needed for superinfection by wild type MuLV. These results indicate that transport of uncleaved env gene-encoded glycoproteins to the cell surface is not a unique attribute to leukemia-producing recombinant of dual tropic MuLVs (Famulari, N. G., and English, J. K. (1981) J. Virol. 40, 971-976) but can also occur with a mutant of ecotropic MuLV.
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PMID:Role of partial proteolysis in processing murine leukemia virus membrane envelope glycoproteins to the cell surface. A viral mutant with uncleaved glycoprotein. 714 94

We have investigated the effects of the tumor promoter 12-0-tetradecanoyl-phorbol-13-acetate (TPA) on plasminogen activator production, hexose transport and metabolism, and the incorporation of choline into the acid soluble pool and into phosphatidylcholine in suspension cultures of mouse L, mouse P388 leukemia, human HeLa, and Chinese hamster ovary cells, and in monolayer cultures of baby hamster kidney (BHK), mouse 3T3, mouse 3T6, and mouse P388D1 macrophage-like cells. BHK, 3T3, P388D1, and P388 cells produced plasminogen activator constitutively, but no significant production was observed in the other cell lines. Plasminogen activator production was induced or stimulated by TPA only in P388 cells (10- to 20-fold by 100 ng TPA/ml). On the other hand, phosphatidylcholine synthesis was stimulated by TPA only in HeLa cells, and hexose transport, as measured with 3-0-methyl-D-glucose, only in 3T3 and P388D1 cells, as well as in human lymphocytes. The stimulation of hexose transport occurred more rapidly than the induction of plasminogen activator production and seemed to be part of the mitogenic response of cells to TPA treatment. A stimulation of deoxyglucose uptake was similarly limited to 3T3 and P388D1 cells. A significant decarboxylation of carbon 1 of deoxyglucose occurred in P388 and P388D1 cells, but not in Novikoff cells, and any decarboxylation that occurred was not stimulated by TPA. The results indicate that the various investigated responses of cells to TPA are unrelated and occur independent of each other. The time courses of the biochemical responses also differ significantly.
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PMID:Lack of correlation between effects of tumor promoter TPA on plasminogen activator production, phosphatidyl choline synthesis, and hexose transport in mammalian cell culture systems. 719 88

Rapid kinetic techniques were employed to measure the transport of the nonmetabolizable hexose, 3-O-methyl-D-glucose, in suspensions of human HeLa cells, mouse L- and P388 leukemia cells, and Chinese hamster ovary cells in zero-trans entry and exit and equilibrium exchange procedures. The kinetic parameters of transport were computed by fitting appropriate integrated rate equations to time courses of transmembrane equilibration of radiolabeled substrate. Transport of all four lines, as in Novikoff rat hepatoma cells, conformed to a simple carrier model with directional symmetry but differential mobility of loaded and empty carrier. As was apparent from a comparison of influx and exchange flux, the loaded carrier of all cell types moved between 4 and 14 times faster than the empty carrier. ATP depletion of the cells by incubation in glucose-free medium containing KCN and iodoacetate had no significant effect on the kinetic properties of the transporter. ATP-depleted cells were used to measure the transport of D-glucose, 2-deoxyglucose, D-galactose, and D-glucosamine in the absence of intracellular metabolism. The differential mobilities of empty carrier and carrier loaded with these hexoses and the efficiency of their transport were equivalent to those observed with 3-O-methylglucose, but the Michaelis-Menten constants for the transport of D-galactose and D-glucosamine were 5-8-fold higher than those for D-glucose, 2-deoxy-D-glucose, and 3-O-methylglucose, which were about equivalent.
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PMID:Broad specificity hexose transport system with differential mobility of loaded and empty carrier, but directional symmetry, is common property of mammalian cell lines. 720 77


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