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)

An adherent cell isotopic staphylococcal protein A test (ISPAT) was used to estimate the abundance of mouse mammary tumor virus (MMTV) gp52 cell surface antigen (CSA)on mammary tumor cells. Protein A assays were first utilized, not strictly as a means of antigen detection, but as a means to determine the kinetics of dexamethasone-mediated changes in gp52 cell surface expression. Results indicated increases in gp52 CSA within 4 h of dexamethasone treatment and maximal levels of antigen expression within 12-24 h after treatment. Comparison of gp52 determinants on dexamethasone-stimulated mammary tumor cells demonstrated a greater abundance on C3H Mm5mt/cl than on GR-MMTV cultures. Parallel antigen assays with gp52 and Rauscher murine leukemia virus (R-MuLV) antisera demonstrated that GR-MMTV cells expressed fewer C-type determinants and thus a more preferential expression of gp52 determinants than other cell lines tested. The gp52/R-MuLV binding ratio was only 2.4:1 for C3H cultures in contrast to 5.7:1 for GR cultures. In addition, a comparison of gp52 expression on viral producer and nonproducer cells provided a quantitative estimate of the extent of expression which occurred in a retrovirus nonproducer culture. Results of ISPAT demonstrated that 75% of the gp52 detected on producer cells was present on nonproducer cultures. Comparison of the expression of gp52 CSA and the release of gp 52 into culture fluids during hormone treatments demonstrated that both assays (ISPAT and gp 52 radioimmunoassay) detect and quantitate coordinate changes in the expression and release of MMTV gp52. In antibody excess, protein A assays provided quantitative estimates of CSA abundance not offered by alternative methods of CSA detection.
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PMID:Estimation of mouse mammary tumor virus gp52 abundance by protein A assay: a comparison of viral antigen expression on C3H and GR mammary tumor cells. 627 4

Spleen cells from mice immunized with Epstein-Barr virus-transformed lymphoblastoid cells (EB-LCL) were used to generate monoclonal antibodies to cell surface antigens associated with the EB virus-transformed state. Radioimmune and immunofluorescence binding assays identified two antibodies, MHM6 and AC2, which reacted consistently with all EB-LCL tested, with a subpopulation of cells in some but not all EB virus genome-positive Burkitt lymphoma lines, but with none of a range of EB virus genome-negative cell lines of lymphoma or leukaemia origin. While MHM6 appeared to bind an EB virus-related antigen, AC2 bound some other cell surface antigen which was also found on a small subpopulation of cells in lymphocyte cultures stimulated with phytohaemagglutinin or with pokeweed mitogen. MHM6 and AC2 recognized single polypeptides with apparent molecular weights of 45 kd and 80 kd respectively as shown by sodium dodecylsulphate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of 125I-labeled cell surface polypeptides immunoprecipitated with these antibodies. These polypeptides were induced on experimentally-infected B cells within 24 h of the expression of the EB virus nuclear antigen, EBNA, at a time known to coincide with the appearance of the lymphocyte-detected membrane antigen, LYDMA. However, saturating concentration of MHM6 and AC2 were unable to protect EB-LCL target cells from lysis by LYDMA-specific cytotoxic T cells in a chromium-release assay.
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PMID:Monoclonal antibodies to Epstein-Barr virus-induced, transformation-associated cell surface antigens: binding patterns and effect upon virus-specific T-cell cytotoxicity. 628 62

DNAs of all inbred mouse strains contain multiple copies (18 to 28 copies per haploid mouse genome) of endogenous xenotropic murine leukemia virus-related sequences detectable by Southern analysis with a xenotropic murine leukemia virus env gene-specific probe. After PvuII digestion, we identified a subset of xenotropic murine leukemia virus-related sequences that are well resolved by agarose gel electrophoresis and can be mapped to specific chromosomes by using recombinant inbred mouse strains. Interestingly, three of six xenotropic proviral loci that we mapped were integrated near genes encoding mouse lymphocyte antigens (Ly-m22, chromosome 1; Ly-m6, chromosome 2; and Ly-m10, chromosome 19) and a fourth xenotropic proviral locus mapped near a gene on chromosome 4 that has a major influence on xenotropic virus cell surface antigen levels. These studies indicate that xenotropic proviral loci are located on many different mouse chromosomes and may be useful markers for molecularly cloning and characterizing regions of the mouse genome important in lymphocyte development.
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PMID:Endogenous xenotropic murine leukemia virus-related sequences map to chromosomal regions encoding mouse lymphocyte antigens. 632 91

The development of leukemia/lymphoma in euthymic and congenitally thymus-deficient (nude) mice infected with Friend murine leukemia virus (Friend MuLV) was investigated; both groups developed fatal leukemias within 2-4 months post-infection but the gross and micropathology of lymphoid organs, coupled with cell-surface marker studies indicated the development of two distinct forms of disease. In euthymic mice one group developed lymphosarcomas manifested by thymoma, hepatosplenomegaly and lymphadenopathy whereas the second group developed splenic leukemias manifested only by hepatosplenomegaly. Analysis of surface markers on spleen cells from mice experiencing lymphosarcomas indicated that the majority of cells were positive for Thy 1.2, Moloney cell surface antigen (MCSA), and viral-coded gp70 and p30 antigens but negative for surface immunoglobulin (sIg). Euthymic mice experiencing splenic leukemias yielded spleen cells negative for Thy 1.2, sIg, and MCSA but positive for gp70 and p30. Nude mice uniformly developed splenic leukemias, spleen cells from which were Thy 1.2, MCSA, gp70 and p30 negative, although the proportion of sIg positive cells was higher than that observed in euthymic mice experiencing splenic leukemias. No correlation between the development of lymphosarcoma vs splenic leukemia and a pattern of ecotropic and/or xenotropic MuLV expression was observed. While ecotropic MuLV expression was equivalent in both euthymic and athymic mice, euthymic mice expressed approx. 10-fold higher levels of xenotropic MuLV than nude mice, however. Collectively the data suggest that infection of mice with Friend MuLV results in the development of two possible forms of disease, lymphosarcoma involving T cells vs splenic leukemia involving B and/or null cells.
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PMID:Phenotypic heterogeneity of leukemias associated with Friend MuLV infection: studies on T-cell lymphomas and null cell leukemias in euthymic and thymus-deficient mice. 633 42

Previously, a system was devised whereby H-2-restricted cytotoxic T lymphocytes could be raised that were specific for tumors induced by endogenous AKR/Gross murine leukemia virus and that displayed the Gross cell surface antigen (GCSA). The generation of such anti-AKR/Gross virus CTL required in vivo priming with allogeneic (H-2 and/or non-H-2 incompatible) GCSA+ tumor cells, followed by in vitro restimulation with H-2-compatible GCSA+ tumor cells. The prototype responder strain of mice was C57BL/6, which is of the H-2b type and which has a low incidence of spontaneous virus-induced leukemia ("low leukemic"). Present experimentation indicates that there is H-2-encoded control of the ability to mount an anti-AKR/Gross virus CTL response. In addition to C57BL/6, all other H-2b strains tested, including C57BL/10, C57L, and 129, were responders. In contrast, H-2k strains of both "high leukemic" (AKR) and "low leukemic" (AKR.Fv-1b and CBA) phenotype appeared to be low- or nonresponders with respect to their ability to generate H-2k-restricted anti-AKR/Gross virus CTL after appropriate stimulation. Furthermore, B6.H-2k congenic mice were also poorly responsive, suggesting that H-2b and H-2k were responder and nonresponder haplotypes, respectively. The finding that (responder X nonresponder)F1, i.e., (B6 X CBA)F1 mice mounted CTL responses to H-2b, but not H-2k, GCSA+ tumors, was consistent with this interpretation and suggested the presence of H-2-encoded dominant immune response genes. The tumors of AKR background that were efficient in the in vivo priming of C57BL/6 mice were relatively inefficient in priming (B6 X CBA)F1 mice for a subsequent in vitro H-2b-restricted anti-AKR/Gross virus CTL response. Because of the similarities in background minor H genes of the AKR and CBA strains, this latter observation was in keeping with the requirement for in vivo stimulation with tumor cell alloantigens in addition to the virus-associated target antigens.
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PMID:Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. I. H-2-encoded dominant gene control. 642 9

To assess whether the presence of a responder H-2b haplotype would be sufficient to allow mice of nonresponder "high leukemic" phenotype to generate syngeneic anti-AKR/Gross virus cytolytic T lymphocytes (CTL), the AKR.H-2b strain was examined. Although capable of mounting vigorous apparent anti-minor histocompatibility-specific CTL responses, AKR.H-2b mice failed to produce anti-viral CTL after a variety of stimulation protocols. In contrast, the "doubly congenic" AKR.H-2b:Fv-1b strain was able to respond with substantial levels of H-2-restricted anti-AKR/Gross virus CTL activity. These results indicated that Fv-1n alleles could exert negative epistatic control over responder H-2b-encoded gene(s). Because the B6.Fv-1n congenic was also able to generate anti-viral CTL indistinguishable from the prototype B6 strain, however, it was apparent that other genes of AKR background were required for the Fv-1n-mediated inhibition in AKR.H-2b mice. The mechanism by which Fv-1 intereacted with other genes to override positive H-2b control appeared to be related to the expression of the CTL-defined, virus-associated antigens by normal AKR.H-2b cells. Thus, AKR.H-2b spleen cells but not thymus cells were able to stimulate the production of B6 anti-AKR/Gross virus CTL and were recognized as target cells by such anti-viral CTL. In contrast, both spleen cells and thymocytes from AKR.H-2b:Fv-1b mice were negative when tested as stimulator or target cells in these assays. In addition, AKR.H-2b but not AKR.H-2b:Fv-1b spleen cells were shown to display serologically defined gp70 determinants and the Gross cell surface antigen. Taking these data together, it appeared that the inhibition of anti-viral CTL responsiveness might be due to tolerance induced by the cell surface expression of virus-associated antigens by normal AKR.H-2b cells. Widespread display of viral antigens, in turn, may have been due to the permissive effects of Fv-1n on the spread of the early arising N-ecotropic, endogenous AKR leukemia virus controlled by other background genes. In this context, the implications of the multi-gene control of anti-AKR/Gross virus CTL production are discussed with respect to the induction of spontaneous leukemia in the high incidence AKR strain.
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PMID:Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. II. Negative control by the Fv-1 locus in AKR mice of responder H-2b haplotype. 642 10

An automatic cell harvester was used in the final step of a cellular radioimmunoassay to collect cell bound anti-rat IgG 125I-F(ab')2. Studies on the reliability of this collection method were performed with antibodies directed against cell surface antigens induced by the Gross murine leukemia virus and produced by immunization of W/Fu rats with the syngeneic (C58NT)D lymphoma. Glutaraldehyde-fixed as well as untreated Gross virus induced lymphoma cells could be used. Similar and specific antibody binding curves were obtained when the cells were incubated with the anti-(C58NT)D serum and anti-rat IgG 125I-F(ab')2 in the presence of 0.1% NaN3. Background levels of non-specific binding of anti-rat 125I-F(ab')2 to mouse lymphoma cells or rat thymocytes were only a few cpm above the background of the gamma-counter. This allowed detection of surface immunoglobulin positive lymphocytes among as few as 30,000 rat splenocytes. In addition, this cellular radioimmunoassay was found to be suitable for the measurement of solubilized cell surface antigen by its capacity to inhibit the binding of the specific antibodies to the target cells.
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PMID:Use of an automatic cell harvester in a cellular radioimmunoassay. 651 63

The leukemia-associated cell surface antigen p 24 is found on normal platelets as well as on Bernard Soulier syndrome and thrombasthenia type I platelets. ALB6 IgG (a monoclonal antibody against p 24) induces the aggregation of platelets from normal donors but not from thrombasthenia. In contrast, ALB6 Fab inhibits platelet aggregation induced by collagen, ADP, thrombin, ionophore A 23187 and ALB6 IgG. The results suggest that ALB6 interferes with a mechanism common to all aggregation pathways; the possible mechanisms are discussed.
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PMID:Characteristics of platelet aggregation induced by the monoclonal antibody ALB6 (acute lymphoblastic leukemia antigen p 24). Inhibition of aggregation by ALB6Fab. 657 11

Expression of cell membrane antigens recognized by antiserum raised against purified Friend murine leukemia virus (Fr-MuLV) envelope glycoprotein (gp71) and by xenotropic MuLV-coded cell surface antigen (XenCSA) specific antibodies was studied in the course of the development of Rauscher erythroleukemia in the spleen of Balb/c mice. DNA content vs immunofluorescence or light scattering of cells were simultaneously analyzed. At early stages of the disease (4-5 days after infection) the gp71 and XenCSA-related antigen expression is enhanced mainly on S-G2/M-phase cells as compared to the majority of G1-phase cells or to the endogenous background of uninfected cells. Later (around 10 days after infection) an approximately ten-fold increased gp71-related antigen density is reached in every phase of the cell cycle. These data show that the virus-induced transition from resting to proliferating state is coupled to enhanced expression of both helper and defective viral env-gene products in the cell membrane of mitotic and G1-phase cells as well.
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PMID:A follow-up study of the development of Rauscher erythroleukemia. 658 53

Cytotoxic T-cells were derived from the peritoneal cavity of a C57BL/6 mouse immunized with BALB/c sarcoma Meth A and from the spleens of BALB/c x C57BL/6 F1 (hereafter called CB6F1) mice immunized with BALB/c leukemia RL male 1. The cells were cultured in interleukin 2 and cloned by limiting dilution, and their specificity was determined by direct tests and competitive inhibition assays. C57BL/6 anti-Meth A effector cells recognized H-2Dd determinants. CB6F1 anti-RL male 1 effector cells recognized a unique cell surface antigen of leukemia RL male 1. The specificity was maintained in long-term culture. The cell surface phenotype of the cloned effector cell lines as determined by absorption analysis was Thy-1.2+, Lyt-1.2+, 2.2+, and 3.2+. Cytotoxicity was blocked at the target cell level by antisera against H-2Dd, but not H-2Dk or H-2b, and at the effector cell level by antisera against Lyt-2.2 and 3.2, but not Lyt-1.2, Ly-5.1 or Thy-1.2.
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PMID:Characterization of interleukin 2-dependent cytotoxic T-cell clones: specificity, cell surface phenotype, and susceptibility to blocking by Lyt antisera. 660 Feb 15


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