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)

Treatment of Rauscher murine leukemia virus lysates with the anionic detergent sodium dodecyl sulfate (SDS) at concentrations between 0.2 to 2.0% SDS per mg of viral protein greatly increased the anodal electrophoretic mobility of p30, the major internal polypeptide. SDS treatment did not reduce p30 antigenicity or cause nonspecific precipitation of normal serum proteins during subsequent immunoanalysis. The increased anodal electrophoretic mobility allowed assay of Rauscher murine leukemia virus p30 by Laurell rocket immunoelectrophoresis. An SDS-facilitated rocket immunoelectrophoresis assay is described that was highly reproducible (coefficient of variability, less than 3.0%) and capable of detecting 125 ng of viral protein. To our knowledge, this is the first report of a quantitative immunoelectrophoretic assay for an oncornavirus antigen. Since SDS binding is a general property of proteins, this method of noncovalently altering electrophoretic mobility appears to be applicable to other antigen-antibody systems.
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PMID:Quantitative immunoelectrophoretic assay for murine oncornavirus p30: noncovalent facilitation by sodium dodecyl sulfate. 90 22

Ultrastructural histochemical evaluation of the surface of normal human blood and bone marrow cells exposed to the pyroantimonate-osmium (PAO) reaction indicated the selective binding of pyroantimonate to certain cations (calcium, magnesium, and possibly sodium) associated with the plasma membrane of neutrophilic leukocytes and their developmental forms. Other leukocytes and their precursors did not exhibit plasma membrane PAO reactivity. The extent of surface binding was related to cell maturity, with maximal labeling evident in the mid and late promyelocytes; decreased binding occurred with subsequent maturation while myeloblasts were nonreactive. This study was initiated to ascertain if histochemical surface modifications of neutrophilic cells occur in certain myeloproliferative disorders. In this regard, we have been able to demonstrate a distinctive defect in the plasma membrane PAO binding characteristics of the leukemic cells in chronic myelocytic leukemia (CML). Limited binding of pyroantimonate to the plasma membrane of the leukemic cell series in four patients with CML contrasted with that of the normal granulocytic cell series and the neutrophilic cells seen in myelomonocytic leukemia (two patients), myelofibrosis (one patient), and acute myelocytic leukemia (three patients). Comparison of surface PAO reactivity of neutrophilic cells in all stages of maturation in two patients with CML in blast crisis revealed that, in the patient with 30% circulating blast cells, PAO reactivity was identical to that noted in CML, while in the patient with 80% circulating blast forms, the PAO reactivity of the maturing neutrophilic cells more nearly resembled that observed in neutrophilic cells from normal individuals. Many neutrophilic cells from patients with myelofibrosis and myelomonocytic leukemia and from one patient in severe blast crisis had large surface deposits of pyroantimonate considered to reflect increased membrane-associated reactive cation.
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PMID:Ultrastructural histochemical alteration of the plasma membrane in chronic myelocytic leukemia. 106 Apr 72

We have labelled the exposed surface glycoproteins of human blood T- and B-lymphocytes and cells from patients with chronic lymphocytic leukemia by the galactose oxidase-tritiated sodium borohydride method. The labelled glycoproteins were separated by polyacrylamide slab gel electrophoresis and visualized by autoradiography. The T- and B-lymphocytes show different and characteristic surface glycoprotein patterns. The surface glycoprotein patterns of the leukemic cells differ from those of normal, non-malignant lymphocytes. A relationship between the altered surface glycoprotein pattern of leukemic cells and the expression of leukemia-associated antigens is discussed.
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PMID:Different surface glycoprotein patterns on human T-, B- and leukemic-lymphocytes. 108 48

We have previously demonstrated that guinea pig alloantisera directed at strain 2 and strain 13 membrane antigens block specific lymphocyte activation in immune response gene-controlled systems. In this communication we describe the partial characterization of the antigens against which these antisera are directed (the 2 and 13 antigens) and, in addition, that of the B antigen which by distribution resembles the human HL-A and mouse H-2 major histocompatibility antigens. Lymphoid cells from strain 2 and strain 13 guinea pigs were surface labeled with 125I by the lactoperoxidase technique. Nonidet P-40 extracts of these labeled cells were precipitated by sandwiches of strain 2 antistrain 13, strain 13 antistrain 2, or outbred anti-B antisera, followed by rabbit antiguinea pig immunoglobulin antisera. Precipitates were dissolved in sodium dodecyl sulfate (SDS) and electrophoresed on SDS polyacrylamide gels. Radioactive peaks representing the 2 and B-cell membrane antigens were obtained from strain 2 lymph node cells, as well as from a B-lymphoid cell population (L2C leukemia cells) and a T-lymphocyte population (STRAIN 2 PERITONEAL EXUDATE LYMPHOCYTES [PELs]). Radioactive peaks representing the 13 and B-cell membrane antigens were obtained from strain 13 lymph node cells and strain 13 PELs. All anti-B precipitates produced two peaks when electrophoresed on SDS polyacrylamide gels; one representing an antigen with a mol wt of approximately 45,000, and one representing an antigen with a mol wt of about 12,000. Both may be components of a single protein. All anti-2 and anti-13 precipitates produced a single peak when electrophoresed on SDS polyacrylamide gels. Both the 2 and 13 antigens were found by this technique to have mol wt of approximately 25,000. By molecular weight criteria, as well as by previously investigated distributional criteria, the B antigen is similar to the human LA and Four antigens, and to the mouse D and K antigens, and the 2 and 13 antigens are similar to the mouse Ia antigens.
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PMID:Guinea pig immune response-related histocompatibility antigens. Partial characterization and distribution. 109 Jun 99

The high-molecular-weight RNA of Moloney murine leukemia virus (MuLV) was analyzed by sedimentation equilibrium ultracentrifugation. Molecular weights of 7.2 x 10(6) and 3.4 x 10(6) were found for the native and subunit forms, respectively, indicating that the native structure is a dimer. S20,w and frictional coefficients were determined for MuLV RNA by analytical velocity centrifugation as a function of ionic strength. The apparent S20,w of native MuLV RNA was 47.3, 57.4, and 66.5 in 0.01, 0.1, and 0.20 M Na+, respectively; the corresponding frictional coefficients were 5.44, 4.48, and 3.87. Native RNA was estimated by circular dichroism to be 85% helical, whereas denatured RNA was 54% helical. Thermal denaturation profiles were obtained from uv absorbance scans. Melting temperatures of 57 and 68 C were obtained for high-molecular-weight RNA in 0.01 M Na+ and 0.122 M Na+, 1mM Mg2+, respectively. van't Hoff plots of the thermal denaturation data gave enthalpies for the helix-coil transition of 21,600 cal (ca. 90,500 J) per mol of cooperatively melting unit in high salt and 19,600 cal (ca. 82,100 J) per mol in low salt, consistent with both base stacking and pairing. The melting of Mu LV RNA occurred over a broad temprange and van't Hoff plots were linear over most of the melting range, indicating a noncooperative process of helix stabilization.
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PMID:Physical properties of moloney murine leukemia virus high-molecular-weight RNA: a two subunit structure. 120 47

The lymphoid leukaemia L 1210 cells of mice were labelled with 125I. The cell homogenates were fractionated and from the microsomal fraction 90 per cent of the radioactive material could be precipitated with perchloric acid, whereas only 4 per cent was precipitated from the soluble fraction. Papain bound with Enzacryl AH released 31 per cent of radioactivity. It was concluded therefrom that the surface proteins of the cells were labelled. Electrophoretic separation of these proteins in polyacrylamide gel with sodium dodecyl sulphate was performed and 6--8 radioactive fractions of surface peptides were found.
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PMID:Radioiodination of L 1210 cells. 123 13

The membrane changes which occur during cellular maturation of erythroid cells have been investigated. The transport of alpha-aminoisobutyric acid, alanine, and N-methylated-alpha-aminoisobutyric acid have been studied in the erythroblastic leukemic cell, the reticulocyte, and the erythrocyte of the Long-Evans rat. The dependence of amino acid transport on extracellular sodium concentration was investigated. Erythrocytes were found to transport these amino acids only by Na-independent systems. The steady state distribution ratio was less than 1. Reticulocytes were found to transport alpha-aminoisobutyric acid and alanine by Na-dependent systems, but only small amounts of N-methylated-alpha-aminoisobutyric acid. Small amounts of these amino acids were transported by Na-independent systems. The steady state distribution ratio was greater than one for Na-dependent transport. The erythroblastic leukemia cell, a model immature erythroid cell, showed marked Na-dependence (greater than 90%) for alpha-aminoisobutyric acid and alanine transport, and greater than 80% for the Na-dependent transport of N-methyl-alpha-aminoisobutyric acid. The steady state distribution ratio for the Na-dependent transport was greater than 4. In the erythroblastic leukemic cell, at least three Na-dependent systems are present: one includes alanine and alpha-aminoisobutyric acid, but excludes N-methyl-alpha-aminoisobutyric acid; one is for alpha-aminoisobutyric acid, alanine and also N-methyl-alpha-aminoisobutyric acid; and one is for N-methyl-alpha-aminoisobutyric acid alone. In the reticulocyte, the number of Na-dependent systems are reduced to two: one for alpha-aminoisobutyric acid and alanine; one for N-methyl-alpha-aminoisobutyric acid. In the erythrocytes, no Na-dependent transport was found. Therefore, maturation of the blast cell to the mature erythrocyte is characterized by a systematic loss in the specificity and number of transport system for amino acids.
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PMID:Maturation of membrane function: transport of amino acid by rat erythroid cells. 124 Jan 4

Purified rat peritoneal mast cells (RMC) and cultured rat basophilic leukemia (RBL) cells were surface labeled with 125I by using lactoperoxidase, incubated with unlabeled rat monoclonal IgE and subjected to solubilization by treatment with Nonidet P-40 (NP-40). With both cell types significant amounts of radioiodinated material could be specifically precipitated by a "sandwich" system consisting of rabbit anti-rat epsilon-chain and goat anti-rabbit Ig. The precipitates were dissociated with sodium dodecyl sulfate (SDS) and urea and subsequently analyzed by SDS-polyacrylamide gel electrophoresis. With RMC three radioactive bands were seen. One corresponded to IgE present on the RMC at the time of isolation. A small band migrating in the region of light chain was seen with both sepcific (anti-IgE) and control precipitates. It showed no demonstrable relationship to IgE. The major radioactive band corresponded to a m.w. of 62,000. This band was dependent upon the presence of IgE and was not found when non-IgE binding control cells were used. With RBL cells, only the IgE-dependent 62,000 dalton peak was present. Saturation of the IgE receptor sites of the RMC or RBL cells before lactoperoxidase labeling almost totally eliminated this radioactive band, indicating that cell-bound IgE rendered this membrane component inaccessible to the radiolabel. These results strongly suggest that this cellular component is identical, at least in part, with the target cell surface receptor for reaginic antibody. The data also further support the hypothesis that the neoplastic RBL cells have a normal surface receptor for IgE.
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PMID:Characterization of the target cell receptor for IgE. II. Polyacrylamide gel analysis of the surface IgE receptor from normal rat mast cells and from rat basophilic leukemia cells. 124 17

The Moloney murine leukemia virus causes thymic leukemias when injected into newborn mice. A major genetic determinant of the thymic disease specificity of the Moloney virus genetically maps to two protein binding sites in the Moloney virus enhancer, the leukemia virus factor b site and the adjacent core site. Point mutations introduced into either of these sites significantly shifts the disease specificity of the Moloney virus from thymic leukemia to erythroleukemia (N. A. Speck, B. Renjifo, E. Golemis, T. Frederickson, J. Hartley, and N. Hopkins, Genes Dev. 4:233-242, 1990). We have purified several polypeptides that bind to the core site in the Moloney virus enhancer. These proteins were purified from calf thymus nuclear extracts by selective pH denaturation, followed by chromatography on heparin-Sepharose, nonspecific double-stranded DNA-cellulose, and core oligonucleotide-coupled affinity columns. We have achieved greater than 13,000-fold purification of the core-binding factors (CBFs), with an overall yield of approximately 19%. Analysis of purified protein fractions by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis reveals more than 10 polypeptides. Each of the polypeptides was recovered from an SDS-polyacrylamide gel, and those in the molecular size range of 19 to 35 kDa were demonstrated to have core-binding activity. The purified CBFs were shown by DNase I footprint analyses to bind the core site in the Moloney virus enhancer specifically, and also to core motifs in the enhancers from a simian immunodeficiency virus, the immunoglobulin mu chain, and T-cell receptor gamma-chain genes.
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PMID:Purification of core-binding factor, a protein that binds the conserved core site in murine leukemia virus enhancers. 130 96

The anti-proliferative effects of selenium were studied both in vivo and in vitro. At a selenium concentration of 0.6 micrograms/ml, cells from patients with ALL-L1, L2 and AML-M1, M3 and M5 were more sensitive than cells from patients with CML. Cells from patients with AML-M2, CLL and leukaemic lymphoma were least sensitive. Normal bone marrow or peripheral blood cells were not sensitive to selenium at this concentration. In the mouse leukaemia models (L797, L615, L7712), the sensitivity of leukaemic cells were: L797 (93% cytotoxicity) greater than L615 (49.7% cytotoxicity) greater than L7712 (4.4% cytotoxicity). Sodium selenite injected i.p. increased the longevity of L797-inoculated mice. Administration of 40 micrograms selenium daily for 7 days resulted in a significant increase in the longevity of mice inoculated with 10(5) L797 cells. However, no remarkable increase of the longevity was observed in either L615- or L7712-inoculated mice after treatment with sodium selenite for 7 days. Treatment of the HL-60 leukaemic cell line with selenium caused a dose- and time-related decrease in DNA, RNA and protein syntheses as measured by [3H]-thymidine, [3H]-uridine and [3H]-leucine uptake respectively. The inhibitory effect of selenium on DNA synthesis was reversed when selenium was removed from the medium, demonstrating that selenium-induced inhibition of DNA synthesis was due to interference with DNA biosynthesis rather than DNA template damage. These results suggest that the anti-leukaemic effect of sodium selenite is associated with inhibition of DNA replication, transcription and translation.
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PMID:The anti-leukaemic effects and the mechanism of sodium selenite. 131 17


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