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 clinical application of an antiserum recognizing common ALL associated antigen (cALL-AG) is very useful in classifying leukemias and diagnosing bone marrow relapse as well as CNS-leukemia. We could demonstrate that sera of common ALL (cALL) patients contain cALL-AG; its partial biochemical characterization is described. The anti cALL serum (cALL-AS) was raised in rabbits with cALL-cells precoated with rabbit antiserum against normal human lymphocytes. After appropriate absorbtion the cALL-AS was highly specific for cALL cells. The isolation of serum cALL-AG was performed by ammoniumsulfat precipitation, gel chromatography and affinity chromatography on agarose lens culinaris hemagglutinin A (lentil lectin). The apparent molecular-weight of the serum glycoprotein is 125 000. Two cALL-AG active structures could be solubilized from cALL cell membrane. The apparent molecular-weights were calculated to be 55 000 and 110 000.
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PMID:[Common ALL-associated antigen on cells and in the serum of common ALL patients: clinical relevance and biochemical characterization (author's transl)]. 28 47

We have labeled surface glycoproteins of normal and malignant human blood leukocytes by the galactose oxidase-NaB3H4 and periodate-NaB3H4 labeling techniques. The labeled glycoproteins were separated by slab gel electrophoresis in the presence of sodium dodecyl sulfate and visualized by fluorography. The different types of normal blood cells could be distinguished by their surface glycoprotein patterns. The surface glycoproteins of cells from patients with acute lymphoblastic, myeloid, or monoblastic leukemia were different from those of normal cells. The leukemic cells could be classified by their surface glycoprotein patterns with respect to their relationships to normal blood cells, and an estimation of their degree of differentiation was obtained.
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PMID:Identification and characterization of normal and malignant human blood leukocytes by surface glycoprotein patterns. 29 63

Human and mouse lymphocytes were surface-labeled by lactoperoxidase-catalyzed iodination, or by galactose oxidase oxidation followed by reduction with tritiated sodium borohydride. The labeled cells were lysed with Nonidet P-40. Proteins binding to Helix pomatia A hemagglutinin (HP) were isolated by affinity chromatography on HP-Sepharose and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography. A major cell surface glycoprotein (apparent mol. wt. 150 000, using reducing conditions) on human lymphocytes was responsible for almost all binding of HP. This protein was present on normal and malignant thymus-derived lymphocytes, e.g. thymocytes, blood T cells and T leukemia cell lines. It was also found on chronic lymphocytic leukemia cells, one null cell leukemia line, one unidentified leukemia line, one lymphoblastoid cell line of B origin and on one stem cell lymphoma line. In contrast, this protein was not found on various B cells at different steps of differentiation, e.g. four B lymphoma lines or one myeloma line. It was also absent from a histiocytic leukemia line. However, two of the four B lymphoma lines and the myeloma line had another HP-binding surface glycoprotein (mol. wt. 200 000) instead of the 150 000 protein. Studies of mouse lymphocytes similarly showed that thymus-derived lymphocytes (normal and malignant) but not normal adult B cells expressed a major HP-binding surface glycoprotein of apparent mol. wt. 130 000 (reducing conditions).
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PMID:Helix pomatia A hemagglutinin: selectivity of binding to lymphocyte surface glycoproteins on T cells and certain B cells. 30 19

The H-2, thymus-leukemia (TL), and Qa-2 antigens of mice are encoded by closely linked genes on murine chromosome 17, and have structural similiarity in that each antigen is borne on a approximately 44,000 dalton molecule associated with beta2 microglobulin (beta2mu). The extensive homology of major histocompatibility complex (MHC) products that exists for the mouse and guinea pig suggested that a similar homology might exist for products of genetic regions closely linked to the MHC. By taking advantage of the selective association of beta2mu with H-2, Qa-2, and TL antigens, and by using the technique of sequential immunoprecipitation, we demonstrated two previously undescribed guinea pig molecules reactive with anti-guinea pig beta2mu. The first molecule was composed of a 36,000 dalton glycoprotein associated with beta2mu and was found on guinea pig thymocytes, but not lymphocytes. The second molecule was composed of a 40,000 dalton glycoprotein associated with beta2mu, and was found on both guinea pig thymocytes and lymphocytes. By structure, chemical composition, association with beta2mu, and tissue distribution, the first molecule is an attractive candidate for the guinea pig homologue of TL antigen, whereas the second fits the criteria for the guinea pig homologue of Qa-2 antigen.
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PMID:Guinea pig homologues of TL and QA-2 antigens. 35 57

Cell-mediated immunity to Moloney murine leukemia virus (M-MuLV) and to tumor-associated surface antigens of leukemia cells induced by the virus was studied with an in vitro migration inhibition factor assay. Spleen cells of C57BL/6N mice at Day 14 following inoculation with Moloney murine sarcoma virus, produced migration inhibition factor in response to M-MuLV. The Moloney murine sarcoma virus-immune spleen cells, however, did not respond to other murine type C viruses, to AKR and Rauscher viruses, or to murine mammary tumor virus. The immune spleen cells also responded specifically to purified glycoprotein with molecular weights of 69,000 and 71,000 and proteins with molecular weights of 30,000 and 12,000, but not to protein with a molecular weight of 10,000, of the homologous M-MuLV. Migration inhibition factor production was also observed in response to soluble 3 M KCl extracts of leukemia cells, MBL-2, induced by M-MuLV. Similarly, the immune spleen cells responded to membrane fractions purified from the MBL-2 cells. Comparable membrane fractions prepared from a Gross virus-induced leukemia, E male G2, and a radiation-induced leukemia, RL male 1, were not active. The tumor-associated surface antigens of MBL-2 membranes could be solubilized by the detergent, Nonident P-40. Thus, C57BL/6N mice inoculated with Moloney murine sarcoma virus developed cell-mediated immunity to envelope and some internal antigens of M-MuLV and also to tumor-associated surface antigens of a tumor induced by this leukemia virus.
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PMID:In vitro studies of cell-mediated immunity to Moloney murine leukemia virus and Moloney leukemia-associated surface antigens. 38 18

Cells infected with a temperature-sensitive mutant (ts-26) of Rauscher murine leukemia virus (R-MuLV) or with wild-type virus were labeled with 35S-methionine, and cell extracts were examined for radioactive polypeptides which could be precipitated by monospecific antisera to viral proteins. When shifted from permissive (31 degrees C) to nonpermissive (39 degrees C) temperature, cells infected with ts-26 rapidly begin to accumulate gPr90enr, the glycoprotein precursor to the membrane envelope glycoprotein gp70 and to the membrane-associated protein p15E. Simultaneously, formation of these mature virion proteins ceases. In addition, lactoperoxidase-catalyzed surface labeling with 125I--iodine indicates that the plasma membrane of cells infected with ts-26 becomes depleted of gp70 antigens at 39 degrees C. Nevertheless, at 39 degrees C these cells release defective MuLVs which lack gp70 and p15E but contain an outer membrane. The released particles also contain an aberrantly processed form of the major virion core protein p30, and many of these virion cores have an unusual immature crescent shape. It has previously been reported that cells infected with the ts-26 mutant of R-MuLV process a 65,000 dalton precursor (Pr65gag) of the virion core proteins more slowly at 39 degrees C than do cells infected with wild-type virus (Stephenson, Tronick and Aaronson, 1975). Although we have confirmed these results, this effect is relatively small and it is known that various alterations of MuLV assembly can lead secondarily to inhibited processing of Pr65gag. We propose that the ts-26 mutant has a primary temperature-sensitive defect in membrane glycoprotein synthesis and that this change causes pleiotropic effects on core morphogenesis.
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PMID:A murine leukemia virus mutant with a temperature-sensitive defect in membrane glycoprotein synthesis. 42 Dec 71

The glycosylated env gene precurosr (Pr80env) of Moloney murine leukemia virus has been isolated by selective immunoprecipitation. Use of the drug tunicamycin to inhibit nascent glycosylation or specific cleavage with endoglycosidase H demonstrated that the precursor contained an apoprotein with a molecular weight of 60,000. The finished virion glycoprotein (gp70) was largely resistant to the action of endoglycosidase H. Chromatography of the glycopeptides of Pr80env in conjunction with endoglycosidase H digestion studies suggested that the precursor contained two distinct major glycosylation sites. Analysis of partial proteolytic cleavage fragments of Pr80env before and after endoglycosidase H treatment placed the two glycosylation sites within a 30,000-dalton region of the apoprotein sequence. Kinetic experiments showed that carbohydrate processing as well as proteolytic cleavage are late steps in the maturation of Pr80env.
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PMID:Structure of the murine leukemia virus envelope glycoprotein precursor. 43 Jun 8

Platelets from a patient with eosinophilic leukaemia were not aggregated by ristocetin. The defect was not corrected by normal human plasma and was due to a platelet abnormality. The patient's platelets also showed a diminished sensitivity to aggregation by bovine factor VIIIVWF. The defect was not associated with a prolonged bleeding time. No abnormalities were detected in ADP, collagen or thrombin-induced platelet aggregation. Biochemical studies showed that the platelets were deficient in sialic acid. This deficiency was associated with a reduced staining for glycoprotein I following SDS-polyacrylamide gel electrophoresis. The results suggest an acquired platelet surface abnormality.
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PMID:A platelet defect in a patient with eosinophilic leukaemia: absent ristocetin-induced platelet aggregation associated with a reduced platelet sialic acid content. 45 58

The major envelope glycoprotein (gp71) purified from Rauscher leukemia virus (R-MuLV) binds efficiently to murine lymphoid cells but not to either murine nonlymphoid cells or lymphoid cells from other species. Binding of 125I-labeled R-MuLV gp71 was competitively inhibited by unlabeled glycoprotein, as well as by whole R-MuLV, but not by murine xenotropic viruses, R-MuLV p30, and several unrelated proteins. Polyacrylamide gel electrophoresis profiles of iodinated gp71 after binding to lymphoid cells were similar to prebound profiles. Antibody to R-MuLV gp71 prevented binding, whereas normal serum had no effect. Adsorption of the glycoprotein to murine lymphoid cells occurs rapidly and is time and temperature dependent. The procedure described is sensitive for detecting the binding activity of approximately 10(4) cells. Binding was proportional up to 2.5 X 10(5) cells per ml and plateaued above 10(7) cells per ml. In the presence of excess R-MuLV gp71, BALB/c thymocytes bound approximately 2.4 X 10(4) molecules per cell.
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PMID:Binding characteristics of Rauscher leukemia virus envelope glycoprotein gp71 to murine lymphoid cells. 56 78

6-Substituted 6-deoxy-L-galactose (L-fucose) derivatives were synthesized as potential antimetabolites of L-fucose. The cytotoxic effects of these compounds were evaluated on P388 leukemia cells in culture. The L-fucose analogues which showed the most potent growth inhibition were the sulfonyl ester, bromo, and iodo derivatives; since these compounds were all capable of alkylation, it is conceivable that their cytotoxic action is a consequence of this property. In agreement with this interpretation, none of the agents synthesized showed specific inhibition of the incorporation of L-[3H]fucose into glycoprotein.
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PMID:Synthesis and biological activity of potential antimetabolites of L-fucose. 57


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