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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During long-term tissue culture of spontaneously transformed clones from BALB/c 3T3 mouse-embryo cells, some clones spontaneously begin to produce high titers of endogenous murine type-C viruses. The antigenic properties of these viruses have been analyzed by indirect immunoelectronmicroscopy and can be classified into two distinguishable populations: (a) BALB/c murine myeloma-associated extracellular viruses that carry a specific envelope antigen, xVEA, different from the typical murine leukemia viral envelope antigens; and (b) previously uncharacterized type-C viruses that have neither xVEA nor the murine leukemia viral envelope antigens. The former produces PC1 antigen and the latter might induce a new cell-surface antigen. Neither of these two populations of BALB/3T3 endogenous type-C viruses was able to infect BALB/c cells but both could infect NIH Swiss cells. A single BALB/3T3 clone, then, can release infectious endogenous type-C viruses with at least two different antigenic properties. We conclude that BALB/c somatic cells contain preexisting genetic information for production of at least closely related but, nevertheless, distinct type-C viruses.
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PMID:Antigenic properties of endogenous type-C viruses from spontaneously transformed clones of BALB-3T3. 435 Nov 84

Cells transformed by murine sarcoma virus have been examined for the presence of a new virus-associated cell-surface antigen by immunoelectron microscopy. A common antigen has been detected on the surface of nonproductively transformed cells that were induced by two different strains of murine sarcoma virus, Kirsten and Moloney. This antigen shows crossreaction with cell lines transformed by murine sarcoma virus that were produced in two different mammalian species, rats and mice. Further, this antigen is distinct from previously described antigens on the surfaces of cells infected by murine leukemia virus, on the viral envelope, and on the surfaces of spontaneously transformed cell lines or cell lines transformed by x-irradiation.
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PMID:Demonstration of a cell-surface antigen associated with murine sarcoma virus by immunoelectron microscopy. 435 2

A new common cell-surface antigen associated with murine and feline C-type RNA leukemia viruses was demonstrated by the use of rabbit antiserum against feline leukemia virus and the indirect membrane immunofluorescence test. Common cell-surface antigen was found in all leukemias of all strains of mice tested, in normal lymphoid tissues of Gross-positive (high incidence of leukemia) mouse strains AKR, AKR.H-2(b), C58, and NZB, in cultured rat fibroblasts infected with Rauscher virus, in cultured feline fibroblasts infected with feline leukemia virus, and in spontaneous feline lymphosarcoma. The antigen was not demonstrable in normal adult and fetal tissues of Gross-negative mouse strains or in tissues and cultured fibroblasts derived from normal rats and normal cats. The immunoferritin study of murine leukemia cells revealed that the antigen was located on the cell surface in discrete areas; budding and C-type RNA viral envelope was not labeled as antigen site. The distribution of common cell-surface antigen on murine and feline leukemias, as well as on normal lymphoid tissues of Gross-positive mouse strains, indicates the presence of an antigen distinct from any cell-surface antigen heretofore shown to be associated with, or specified by, mammalian C-type RNA viruses.
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PMID:Common cell-surface antigen associated with murine and feline C-type RNA leukemia viruses. 435 60

Preparations of mouse interferon enhanced the expression of surface antigens of murine leukemia L 1210 cells, as determined by their alloantibody-absorbing capacity. The factor responsible for the enhancement of surface antigen expression could not be dissociated from the antiviral activity of interferon by standard physicochemical means. Likewise, interferon did not increase the antibody-absorbing capacity of an interferon-resistant subline of L 1210 cells. We conclude that interferon treatment of L 1210 cells is accompanied by modifications of the cell surface.
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PMID:Enhancement by interferon of the expression of surface antigens on murine leukemia L 1210 cells. 451 33

The expression of Moloney leukemia virus on the surface of a viral-induced lymphoma cell, availability of the virus to anti-viral antibody, and the nature and extent of activation of the complement system during the cell cycle were studied in vitro. Viral antigen was present on the cell surface, accessible to antibody, and was able to activate complement in the presence of antibody throughout all cellular growth phases, while cytotoxicity was confined to the G(1) phase of cell growth. In addition, when cells were arrested in metaphase, viral antigen could be demonstrated on the cell surface by immunofluorescence, and budding virus was seen by electron microscopy. All nine components of complement were activated on the addition of antibody throughout the cell cycle. Additional experiments indicated that in the presence of antibody, C3 and/or C4 were immunospecifically bound to viral-induced lymphoma cells throughout the cell cycle as a result of complement activation. These results indicate that the inability to lyse the cells in the presence of specific anti-viral antibody and complement during the logarithmic phase of cell growth is not due to the lack of expression of Moloney virus antigen(s) on the cell surface, inaccessibility of this surface antigen(s) to antibody, or failure to activate the complement effector system.
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PMID:Cell cycle-dependent immune lysis of Moloney virus-transformed lymphocytes: presence of viral antigen, accessibility to antibody, and complement activation. 494 33

Some murine sarcoma virus (MSV)-transformed mouse 3T3 cells contain the MSV genome in the absence of infectious helper murine leukemia virus (MuLV) and MSV production. These cells, designated S+L- (sarcoma positive, leukemia negative), were analyzed for the presence of a possible MSV-determined membrane antigen by the mixed hemadsorption test and in vitro lymphocyte cytotoxicity assay. Two different serological approaches were used: (a) isoantibody-free sera were obtained by immunizing with MSV of syngeneic origin or by allowing primary, autologous MSV sarcomas to regress, or (b) alloantisera obtained by immunizing C57BL mice with S+L- cells were absorbed with the corresponding nontransformed 3T3 cells until all activity against 3T3 had been removed. While MuLV-superinfected S+L- cells and a culture line of an MSV sarcoma known to produce both MSV and MLV were highly reactive, normal 3T3 and S+L- cells were negative. Similarly, lymph node cells from MSV immune mice or rats did not kill S+L- cells, although they were cytotoxic against target cells known to carry MuLV-associated antigens. Thus, the present study gives no positive evidence for the existence of any MSV-induced new surface antigen in the transformed target cell, known to carry the viral genome.
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PMID:Lack of distinctive surface antigen on cells transformed by murine sarcoma virus. 504 15

The hybrid-antibody method of locating cell-surface antigens in electron micrographs, with either ferritin or southern bean mosaic virus as the visual marker, was applied to the cells of a transplanted murine leukemia induced by Gross virus. The two antigens studied were (a) G (Gross) cell-surface antigen, which is a specific component of cells infected with Gross virus and is identified by cytotoxic hyperimmune C57BL/6 antiserum, and (b) H-2 antigen, which is the major histocompatibility determinant of the mouse. Both antigens were represented on the cell surface in discrete circumscribed areas. Neither antigen was present on free Gross virions or on virions in the process of budding from the cell surface. Thus G cell-surface antigen identified by C57BL mouse cytotoxic antiserum is not a constituent of the viral envelope, which accounts for the poor virus-neutralizing capacity of such antibody. Virus maturation may take place preferentially at regions of the cell surface where H-2 and G antigens are absent, for budding was seldom seen in H-2(+) sectors and never convincingly in G(+) sectors. In other experiments, serum from an untreated NZB mice aged 16 months gave labeling of the virion only, showing that this mouse strain, in contrast to C57BL and other strains, forms antibody to envelope antigen of Gross virus.
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PMID:G (Gross) and H-2 cell-surface antigens: location on Gross leukemia cells by electron microscopy with visually labeled antibody. 526 38

The human T-cell leukaemia/lymphoma virus (HTLV) is an exogenous retrovirus which has been associated with adult T-cell leukaemia/lymphoma (ATL). This malignancy of T lymphocytes is endemic to southern Japan, the West Indies, and to a lesser extent, the Middle East, Central Africa and the southeastern United States. ATL cells from patients of diverse geographical origins have been found to be infected with HTLV-1 (ref.6). HTLV is normally tropic for mature T lymphocytes, especially those expressing the helper-inducer surface antigen phenotype (OKT4 or Leu-3-positive), and the neoplastic T cells infected with HTLV generally express receptors for T-cell growth factor (detected by reactivity with anti-Tac antibody). However, we report here the isolation of a HTLV-infected B-lymphocyte clone from the peripheral blood of a patient with ATL. This clone is cytogenetically normal and is not infected with Epstein-Barr virus (EBV). Co-culture of cells from this clone with cord blood lymphocytes resulted in transmission of HTLV and the immortalization of either T or B lymphocytes. These results suggest that HTLV may be associated with a broader range of host cells than previously recognized.
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PMID:Isolation of HTLV-transformed B-lymphocyte clone from a patient with HTLV-associated adult T-cell leukaemia. 608 61

Simultaneous detection of specific surface markers by immunogold and intracellular peroxidase activity was determined ultrastructurally in normal and leukaemic progenitors of platelets, erythrocytes and granulocytes. A new method of fixation was employed to preserve platelet peroxidase activity. Monoclonal antibodies to platelet glycoproteins labelled exclusively platelet peroxidase (PPO) positive cells, i.e. platelets, megakaryocytes and promegakaryoblasts (PMKB). In acute megakaryoblastic leukaemia, most PMKB possessed both markers while a few PMKB identified by PPO did not bind monoclonal antibodies. This result suggests that PPO appears earlier in maturation than platelet glycoproteins. Although all glycoproteins (GP) displayed fewer sites in PMKB than platelets, GP Ib was often observed in more mature megakaryocytes. Surface (glycophorin A) and intracytoplasmic markers including ferritin, intra-mitrochondrial iron and diffuse peroxidase activity due to haemoglobin of erythroid progenitors, appeared simultaneously. The number of glycophorin A sites increased with maturation. In leukaemia involving PMKB and proerythroblasts, the surface markers were coincident with the localization of peroxidase activity; glycophorin A was always absent from blasts which exhibited PPO activity localized in endoplasmic reticulum. Platelet glycoproteins were never expressed in any other cell lineage. The myeloid surface antigen was present on normal late neutrophilic promyelocytes after the cessation of myeloperoxidase synthesis. In some cases of M1 and M2 AML (FAB classification), labelling was identical to normal cells while in others the antigen appeared earlier than normal. Our findings show that the surface phenotype of blasts from non-lymphoid leukaemia and the intracellular peroxidase activity of a given cell type can be simultaneously demonstrated and analysed by electron microscopy.
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PMID:Simultaneous detection of membrane markers with monoclonal antibodies and peroxidatic activities in leukaemia: ultrastructural analysis using a new method of fixation preserving the platelet peroxidase. 609 46

A monoclonal antibody, PVR-11, was obtained after hybridization of X63Ag8.653 murine myeloma cells with spleen cells from a mouse immunized with human lymphocytes. It recognizes a 175,000- to 185,000-dalton surface antigen present on approximately 80% of normal human peripheral T lymphocytes, 50% of non-T non-B cells, and less than 10% of B cells as determined by complement-dependent microcytotoxicity. It is also present on various leukemia T cells, on some but not all T lymphoblastoid cell lines, and on a small fraction of some B lymphoblastoid cell lines. Some B-cell chronic lymphocytic leukemia cells also express the PVR-11 antigen. Functional analysis of normal human T lymphocytes demonstrated that the PVR-11-depleted T-cell subset contains the precursors of both cytotoxic and suppressor cells but lacks helper cells. On the other hand, cytotoxic effector T cells express the PVR-11 antigen. These results demonstrate that antigenic determinants with relatively wide tissue distribution can dissect functionally distinct human immunoregulatory T-cell subsets.
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PMID:Dissection of distinct human immunoregulatory T-cell subsets by a monoclonal antibody recognizing a cell surface antigen with wide tissue distribution. 626 38


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