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)

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

Antisera have been raised in rabbits to the lymphoblastoid cell line NALM 1 precoated with anti-lymphocyte serum (ALS). Following absorption with chronic lymphocytic leukemia cells (CLL) the antisera reacted mainly with acute lymphocytic leukemia (ALL) cells, and were very similar in specificity to antisera raised to ALL cells precoated with ALS. Leukemia cells from the following numbers of patients were positive for the anti-NALM 1 sera in a complement-dependent cytotoxicity test; 11/14 ALL, 3/15 acute myelocytic leukemia (AML), 1/5 chronic myelocytic leukemia (CML) and 0/8 CLL. Normal B and T peripheral blood lymphocytes were negative. The titer of the anti-NALM 1 sera against positive cells was 1:64 to 1:256 whereas the undiluted sera did not react with negative cells. Ten out of 11 of the positive ALL cells were of the non-B non-T type. However, cells from 1/4 T ALL patients and a cultured T ALL line 8402 were also positive. Six of 12 cultured lymphoblastoid cell lines were positive, all of which were of malignant origin. The molecular weight of the ALL antigen detected by anti-NALM-1 serum was determined by immunoprecipitation and sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis (PAGE) to be approximately 98,000 daltons.
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PMID:Heteroantiserum against acute lymphocytic leukemia raised to the lymphoblastoid cell line NALM-1. 30 68

A competitive radioimmunoprecipitation method was developed for the quantitation of human thymus-leukemia-associated antigen (HThy-L) isolated from human thymus tissue. Antisera to the antigen were raised by immunization of rabbits with purified fractions of HThy-L. The antigen was labeled with 125l by means of a modification of the lactoperoxidase technique and subjected to Sephadex G-100 gel filtration. Analysis of fractions eluted from this column by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed two labeled components with apparent molecular weights of 45,000 and 25,000 daltons, respectively. Immunoprecipitation with anti-HThy-L antiserum demonstrated directly that the 45,000-dalton component carried HThy-L antigenicity. This fraction served as the source of labeled antigen in a competitive radioimmunoassay that permitted the detection of approximately 1 ng HThy-L. With the use of this assay, we confirmed quantitatively that the highest amounts of HThy-L were found in extracts of thymocytes, normal thymus tissues, and lymphoblasts for T-cell lines.
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PMID:Radioimmunoassay for human thymus-leukemia-associated antigen. 31 Sep 9

Thymus-leukemia (TL) antigens are expressed in murine lymphocytes under strict developmental regulation. To elucidate the molecular basis of TL expression, we have identified the molecular species that react with TL antiserum. At least three species can be resolved by metabolic radiolabeling of thymocytes and ASL1 leukemia cells, lysis, immune precipitation, and sodium dodecyl sulfate-polyacrylamide. After a brief incubation with [35S]methionine, the only radioactive molecule recognized by TL antiserum is a homogeneous species with an apparent Mr of 45,000 daltons. This molecule, 45K TL, includes high-mannose-type carbohydrate attached to a 45,000 dalton glycosidase-resistant backbone. In this form, 45K, it is never exposed on the cell surface. If pulse-labeled cells are further incubated with nonradioactive methionine before lysis, however, radioactivity disappears from the 45K TL species and appears in the slower migrating species 46K and 48K TL. Thus, 46K and 48K appear to represent products generated from the 45K TL precursor by posttranslational modification. These TL forms are displayed on the cell surface; they lack high-mannose carbohydrate but evidently include acidic complex-type carbohydrate. Normal thymocytes from Qa:Tla-negative mice lack not only the surface forms of TL but also the intracellular 45K TL form. Peripheral lymphoid cells of Qa:Tla-positive mice synthesize none of these TL species. But the TL antiserum, which contains Qa antibody, recognizes a distinct gene product in spleen and thymus of Qa-Tla-positive mice. In its pulse-labeled form, this molecule, which may represent Qa-1, has an apparent Mr of 44,000 daltons, and consists of a glycosidase-resistant polypeptide core of only 35,000 daltons linked to more high mannose carbohydrate than 45K TL.
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PMID:Synthesis and processing of molecules bearing thymus leukemia antigen. 31 85

5-Fluoro-1,3-oxazine-2,6(3H)-dione (3-oxa-FU) was synthesized by reacting 3-oxauracil with fluoroxytrifluoromethane and decomposing the adduct in the presence of a catalytic amount of Et3N. 5-Methyl-1,3-oxazine-2,6(3H)-dione (3-oxathymine) was prepared by polyphosphoric acid catalyzed ring closure of beta-(N-ethoxycarbonylamino)-2-methacrylic acid and by treatment of citraconimide with sodium hypochlorite. As determined in vitro, 3-oxa-FU was markedly inhibitory to S. faecium (ID50 = 9 X 10(-8) M) and E. coli (ID50 = 1 X 10(-7) M) but was less active against leukemia L-1210 cells (ID50 = 1 X 10(-5) M). At 1 x 10(-4) M, 3-oxathymine was inactive in these cell systems. Inhibition of the growth of S. faecium by 3-oxa-FU was reversed competitively by the natural pyrimidines. The relatively rapid hydrolysis of the compounds in the growth media is a major factor in determining their biological effectiveness.
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PMID:Synthesis and biological activity of 5-fluoro- and 5-methyl-1,3-oxazine-2,6(3H)-dione. 37 35

In an aseptic microbiological assay of folate compounds and their breakdown compounds, using Lactobacillus casei, Streptococcus faecalis, and Pediococcus cerevisiae, 4a-hydroxy-5methyl-4,5,6,7-tetrahydrofolate and 5-methyl-5,8-dihydrofolate were inactive under all conditions to all three organisms and 5-methyl-5,6-dihydrofolate was inactive unless ascorbate was present in the incubation medium, and then only to L. casei. 5-Methyltetrahydrofolate was active only for L. casei, and activity in purified samples to S. faecalis was due to trace amounts of folic acid. Analysis of S. faecalis values in the serum in normal subjects and in patients with various disorders showed that levels of 10-formyltetrahydrofolate are raised in coeliac disease, leukaemia, rheumatoid arthritis, and schizophrenia. 5-Methyltetrahydrofolate is readily absorbed by normal human subjects and by patients with pernicious anaemia but poorly absorbed by patients with coeliac disease or leukaemia. 5-Methyl-5,6-dihydrofolate was quickly absorbed by normal human subjects, being reflected by a considerably raised level of 5-methyltetrahydrofolate in serum when sodium bicarbonate was given by mouth before the 5-methyl-5,6-dihydrofolate. These higher levels were comparable to those in patients with pernicious anaemia after oral administration of 5-methyl-5,6-dihydrofolate. Oral 5-methyl-5,8-dihydrofolate and 4a-hydroxy-5-methyl-tetrahydrofolate did not appear as microbiologically active folates in the serum. The findings of this study suggest that the availability for biological utilisation of the major dietary folate compounds will depend on the amount of gastric acidity and of ascorbate in the intestinal chyme. Many may be unavailable for metabolic utilization in the body.
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PMID:Serum folates in man. 40 3

Reports proposing that the cell or origin of "hairy cell" leukemia (leukemic reticuloendotheliosis) is a B lymphocyte have been based primarily on the presence of surface immunoglobulin markers, frequently in "cap" form. Most of the immunoglobulin markers in this series of patients with hairy cell leukemia were multiclass, but were present in cap form under conditions not usually inducing cap formation in normal or leukemic human lymphocytes. In five cases the authors were able to remove these surface immunoglobulins by trypsinization or overnight incubation in serum-free tissue-culture medium. There was no evidence of synthesis of surface immunoglobulins in these cases following incubation in serum-free tissue-culture medium; however, surface immunoglobulins could again be detected after subsequent reintroduction of these hairy cells into the patients' own sera. The peculiar cap formation could not be prevented with sodium azide, a standard inhibitor of cap formation. Phagocytized latex particles and neutral red dye produced similar caplike structures. These findings suggest that hairy cells readily adsorb and pinocytose circulating immunoglobulins, but do not synthesize them.
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PMID:Functional studies of hairy cell leukemia (leukemic reticuloendotheliosis). 43 32

Immunochemical studies of murine thymus-leukemia antigens (TLA) have confirmed that the subunit structure consists of a 45,000-dalton heavy chain and a beta 2 microglobulin (beta 2m) light chain. Similar structural features are exhibited by the TLA from thymocytes of Tlaa, Tlac, Tlad, and a leukemia cell derived from C57BL/6, a Tlab strain. In addition to the similar subunit structure from the four haplotypes, each TLA shows a similar pattern of trypsin proteolysis. This procedure yields a major heavy chain cleavage product of approximately 37,000 daltons that remains associated with beta 2m and retains most or all of the antigenic determinants of the intact TLA. Evidence is presented that TLA do not exhibit Fc receptor properties, nor do they adsorb to murine leukemia virus antigens under the conditions of isolation for analysis on polyacrylamide gel electrophoresis (PAGE) in sodium dodecyl sulfate (SDS). Taken together these findings strongly support the hypothesis that TLA comprise a family of chemically similar antigens belonging to a structurally and genetically related group that includes H-2D, H-2K, and Qa-2,3.
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PMID:Shared chemical properties of different murine thymus-leukemia antigens. 44 10

Capping, independent of metabolic energy, of surface immunoglobulin (S-Ig) on 'Hairy cells' from patients with Hairy cell leukaemia (HCL) is described. As controls leukaemic cells from a patient with a prolymphocytic leukaemia (PLL) and blood lymphocytes from healthy individuals were used. The specificity of the energy-independent capping of the HCL-cells as compared to the controls was tested by incubation of the cells at 4 degrees C in the presence of 0.1 M sodium azide with different FITC-labelled ligands. In order to find an explanation for this phenomenon, the influence of cytochalasin B, colchicine and the combination of both drugs on capping of S-Ig and concanavalin (Con-A)-receptors at 37 degrees C was investigated. Furthermore the effect of Con A on S-Ig capping and vice versa was studied. The results show that only S-Ig on HCL cells could form caps at 4 degrees C in the presence of sodium-azide. Cytochalasin B alone induced a strong inhibition of Con A capping on all 3 cell types, whereas S-Ig capping was unaffected. Colchicine alone had practically no effect. Anti-Ig inhibited subsequent patch and cap formation with Con A on both HCL cells and PLL cells, whereas Con A caps and patches were redistributed by anti-Ig on PLL cells, but not on HCL cells. Conversely, Con A could link S-Ig to other receptors, leading to inhibition of S-Ig capping at 4 degrees C on HCL cells and to co-capping of S-Ig at 37 degrees C on both cell types. In addition Con A induced redistribution of S-Ig caps. The combination of co-capping of S-Ig by Con A, followed by redistribution of the caps by FITC-anti-Ig simulated inhibition of S-Ig capping by Con A on PLL cells. The major conclusions are: in some cases inhibition of capping may actually be caused by redistribution of caps; the energy-independent capping cannot be explained by free diffusion of S-Ig in the membrane through lack of any connexion with receptor-mobility regulating systems. It is proposed that the energy requirement of capping is needed to inactivate a specific mechanism,w which restrains receptor mobility and which is non-operative in HCL cells.
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PMID:Capping of surface immunoglobulin on 'hairy cells' is independent of energy production. 45 18

Post-translational modifications of retrovirus gag gene-encoded polyproteins include proteolytic cleavage, phosphorylation, and glycosylation. To study the sequence of these events, we labeled JLS-V9 cells chronically infected with Rauscher murine leukemia virus in pulse-chase experiments with the radioactive precursors [35S]methionine, [14C]mannose, [3H]glucosamine, and [32P]phosphate. Newly synthesized gag polyproteins which incorporated label, and the modified products derived from them, were identified by immunoprecipitation of cell lysates with anti-p30 rabbit serum, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Pulse-chase experiments were carried out in the presence as well as in the absence of tunicamycin, an inhibitor of glycosylation. Among the three major polyproteins synthesized in the absence of tunicamycin, two were found to be glycosylated but not phosphorylated. These were designated gPr80gag and gP94gag. Both shared identical [35S]methionine peptides with Pr65gag and p30. Of the two nonglycosylated precursors, Pr65gag and Pr75gag, only Pr65gag was found to be detectably phosphorylated, and Pr75gag could be readily identified only when glycosylation was inhibited. On the basis of these results, a scheme for the post-translational modification of gag polyproteins is proposed. According to this scheme the gag gene-encoded polyproteins are processed from a common precursor, Pr75gag, by two divergent pathways: one leading through the intermediate Pr65gag to internal virion components via cleavage and phosphorylation and the other via tunicamycin-sensitive mannosylation to the intermediate gPr80gag, which is further glycosylated to yield cell surface polyprotein gP94gag.
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PMID:Post-translational modification of Rauscher leukemia virus precursor polyproteins encoded by the gag gene. 48 Apr 54


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