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)

Monoclonal antibodies were raised against a laboratory derived variant of the Raji Burkitt lymphoma cell line. We have characterized two of these antibodies by screening on haematopoietic cell lines, and frozen sections of both reactive and neoplastic lymphoid tissue, and found reactivity with separate cellular components of lymphoid follicles. Monoclonal FW37.4.D5 reacts in section specifically with follicular dendritic reticular cells. Monoclonal 35.1C5 reacts with a subpopulation of splenic marginal zone, and lymph node mantle zone, B lymphocytes, but stains only rare cells within germinal centres. This monoclonal is operationally B lymphocyte specific, distinguishing an 'intermediate' B cell subset, represented in lymphoma by B chronic lymphocytic leukaemia, B hairy cell leukaemia and centrocytic lymphoma.
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PMID:Two monoclonal antibodies raised against a Burkitt lymphoma cell line recognise different cell types within lymphoid follicles. 387 87

The human T leukemia line Jurkat maintains functional characteristics of normal T cells in responding to inducing stimuli by the release of interleukin 2 (IL 2). Presence of a phorbol ester during stimulation eliminated the requirement for specialized accessory cells in the response to cell mitogenic agents such as the lectin concanavalin A or treatment with neuraminidase and galactose oxidase. Antibodies directed against the T cell receptor-associated antigen T3 served as efficient stimuli, especially if aided by agents that cross-link immunoglobulin, indicating that a triggering signal is received by a T cell via aggregation of its antigen receptor complex. A Burkitt lymphoma cell line, Raji, was found to selectively trigger Jurkat cells, suggesting the ability of those cells to respond to certain foreign stimuli. The Jurkat cell line has been instrumental in the purification of IL 2 and cloning of the corresponding gene. Our data suggest it can also serve as a useful model for induction of T cell responses.
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PMID:Analysis of human T lymphocyte activation in a T cell tumor model system. 387 19

A simple and convenient method for efficiently establishing 8-azaguanine-resistant mutant leukemia and myeloma cell lines (for example, the T cell lines Jurkat and CCRF-CEM, human myeloid/macrophage-like cell lines HL60 and U937, Burkitt lymphoma line Raji and the human myeloma line RPMI 8226), is described. The method relies on culturing the cell lines in RPMI 1640 medium containing 8-azaguanine and supplemented with 15% heat-inactivated fetal calf serum and large amounts of amino acids and vitamins, and removes the necessity for pretreatment with mutagenic reagents such as ethyl methylsulfonate or X-irradiation. The possibility of obtaining mutant cell lines using the method described here is about 15 times greater than using media without high levels of amino acids and vitamins. Hybridomas produced between mitogen-activated human peripheral blood lymphocytes and an 8-azaguanine-resistant Jurkat mutant cell line (established by this method) were shown to produce soluble T cell-derived macrophage activating factor (MAF)-like material.
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PMID:A simple method for efficiently establishing 8-azaguanine-resistant mutant human leukemia and myeloma cell lines. 390 63

The growth inhibitory activity of human recombinant leucocyte A interferon (Ro22-8181: alpha-interferon) against 23 human cultured cell lines derived from leukemias and lymphomas was measured quantitatively by regrowth assay. Daudi cells were the most sensitive to it. Two T-cell lines (RPMI-8402, HUT78), three B-cell lines (Raji, Ly16, A3/Kawakami), one non-T, non-B acute lymphoblastic leukemia (ALL) cell line (KOPN-1) and three myelomonocytoid cell lines (U937, THP-1, ML-1) were moderately or slightly sensitive. Although the levels of sensitivity of these cell lines were different, cells could be killed by the recombinant alpha-interferon. Morphological changes in the sensitive cells treated with it were decreases in mitosis, pyknosis and fragmentation of the cells. Thirteen other cultured cell lines were not sensitive. The results indicated that the growth inhibitory activity of recombinant alpha-interferon is not always cell lineage-specific. There were only three cell lines whose sensitivity, expressed by the concentration required for 90% growth inhibition, was less than the several hundred units per milliliter that has usually been obtained as blood levels in clinical trials. These three included one of 10 T-cell lines and two of seven B-cell lines; none of six non-T, non-B ALL and myelomonocytoid cell lines were that sensitive. Among virus-associated cell lines, only Epstein-Barr virus-associated B-cell lines were sensitive to the interferon; adult T-cell leukemia virus-associated T-cell lines were not sensitive. It was demonstrated that recombinant alpha-interferon has a time-dependent, but not a concentration-dependent cytocidal action, indicating that optimal therapeutic schedules of recombinant alpha-interferon for cancer may be daily long-term treatment, not single or short-term large-dose therapy.
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PMID:Time-dependent cytotoxic action of human recombinant alpha-interferon (Ro22-8181) in vitro and the sensitivity of various cultured leukemia and lymphoma cell lines to it. 398 16

A human leukemia-associated antigen (LAA) has been identified by immunofluorescence and electrophoretic analyses. LAA was detected on the surfaces of cells from patients with acute lymphocytic leukemia (ALL) as well as on the surfaces of leukemia cells from the established cell lines NALM-1, NALM-16, MOLT-4, CCRF-CEM, and RPMI 8402. The antigen was not detected on BALM-1 or Raji cells (established B-cell lines), bone marrow cells from ALL patients in remission, or on blood lymphocytes from normal donors. This antigen was most frequently associated with common ALL (cALL); however, cells from 2 of 12 patients with T-cell ALL and 1 patient with B-cell ALL also expressed this antigen. Under reduced conditions, the antigen had an approximate molecular mass of 100,000 daltons as determined by sodium dodecyl sulfate--polyacrylamide gel electrophoresis and autoradiographic analysis and appeared to be the same cALL antigen that has recently been described by others. The probability that LAA is a normal differentiation antigen was discussed.
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PMID:Identification of a leukemia-associated antigen of human acute lymphocytic leukemia. 615 21

A human leukemia-associated differentiation antigen has been identified by a monoclonal antibody (A12) raised to the lymphoblastoid cell line NALM-1. The A12 antigen was expressed on the surface of leukemic cells from patients with common acute lymphoblastic leukemia (c-ALL) as well as on cells of the hematopoietic cell lines NALM-1, Reh-6, Raji, Daudi, CEM, and 8402 as determined by an antibody-binding radioimmunoassay, as well as by indirect immunofluorescence and FACS analysis. This antigen was not detected on normal blood lymphocytes, normal bone-marrow cells or leukemic cells from patients with acute myeloid leukemia (AML). The A12 antigen had an apparent molecular weight of 100 kD as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and appeared to be related to if not identical with the acute lymphoblastic leukemia antigen CALLA described by others. Cross-blocking experiments indicated that preincubation of NALM-1 cells with antibody A12 or J5 (anti-CALLA) could block subsequent binding of 125I-labeled A12 and J5 antibody. These results suggest that the two monoclonal antibodies recognize identical or closely located antigenic sites. The surface membrane expression of A12 antigen in NALM-1 cells was modulated when the cells were cultured in the presence of A12 antibody. Under these conditions, the expression of Ia antigens was unaffected. Re-expression of A12 antigen occurred within 24 h after transfer of the modulated cells into medium devoid of monoclonal antibody.
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PMID:Characterization of a monoclonal antibody (A12) that defines a human acute lymphoblastic leukemia-associated differentiation antigen. 620 73

Cats were classified into 4 categories by immunofluorescence antibody assay for the presence of feline leukemia virus (FeLV) and histologically as a) normal, FeLV-, b) normal, FeLV+, c) lymphosarcoma (LSA), FeLV+, and d) LSA, FeLV-. Determinations by Raji cell radioimmunoassay modified for cat serum revealed circulating immune complex (CIC) levels of healthy cats to be less than or equal to 50 micrograms equivalent aggregated cat immunoglobulin/ml (microgram/ml). In contrast, sera of cats in groups b, c, and d all contained significantly higher CIC levels (up to 12,000 micrograms/ml) associated with marked hypocomplementemia and C activation occurring via the classical pathway. Sera from FeLV+, LSA+ cats with high levels of CIC and sera of healthy cats were fractionated according to size and bouyant density by centrifugation through 10 to 40% sucrose gradients. Analysis of fractions from LSA+, FeLV+ sera revealed that both immune complexes (ICs), FeLV reverse transcriptase (RT), and IgG were present in fractions corresponding to a bouyant density of 1.15 to 1.18 g/ml. The CIC containing fractions activated C by the classical pathway. Sera from normal cats did not have CIC or RT and none of the fractions activated the classical pathway. These data suggest that vital antigen-antibody complexes are present in sera of viremic cats with LSA and these complexes activate the C system.
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PMID:Circulating immune complexes associated with naturally occurring lymphosarcoma in pet cats. 625 67

Four new somatic cell hybrids were obtained by fusion of various Burkitt's lymphoma (BL)-derived cell lines that had different selective markers: Raji-P3HR-1, Daudi-Raji, and a P3HR-1-P3HR-1 "autohybrid" derived from two P3HR-1 sublines. In addition, a hybrid was obtained between the Daudi (BL) line and the human leukemia cell line K562. The hybrids were extensively characterized by means of chromosome, isozyme, and HLA surface markers. The phenotypic differences between the parent cell lines allowed some conclusions with respect to the expression of latent Epstein-Barr virus (EBV) genomes, C3 and EBV receptors, and of immunoglobulin and beta 2-microglobulin-HLA expression as well as the influence of the leukemia cell (K562) genome on B-cell properties in the Daudi-K562 hybrid. B-cell and differentiated markers of these hybrids were characterized. High-level expression dominated for the marker C3 and EBV receptors, which showed a good correlation coefficient of 0.84, as was true for Fc receptors and surface immunoglobulin. The Daudi-K562 hybrid showed loss of all B-cell markers but retention of the leukemia cell markers (e.g., hemoglobin synthesis).
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PMID:Human lymphoma-lymphoma hybrids and lymphoma-leukemia hybrids. I. Isolation, characterization, cell surface markers, and B-cell markers. 627 87

In addition to the spontaneous expression of markers of the early and late phases of the viral cycle [Epstein-Barr virus (EBV), early viral cycle antigens (EA), and viral capsid antigen (VCA)] by a Panel of hybrid cell lines derived by fusion of human hematopoietic cell lines, the induction of these markers by three chemical inducers [5-iodo-2'-deoxyuridine, the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA), and sodium butyrate] were analyzed. A variant of the prototype producer of lytic EBV, P3HR-1 (PICAT) was observed to show consistent low spontaneous and induced production of EA and VCA as compared to the P3HR-1 line from which it was derived. An "autohybrid" (PICATPO-1) between these two lines showed a low production of VCA. Hybrids between Raji and P3HR-1 sublines (RUD-PICAT-1 and RUDPUT-2) showed reduced expression of EBV antigens. Both hybrids were capable of VCA expression, in contrast to the Raji parent that expressed EA but not VCA. A new Raji-Daudi hybrid (DITRUD-1) expressed spontaneous and induced EA and VCA at levels intermediate between its two parents. A different type of hybrid was derived from a Daudi subline and the K562 leukemia cell line (DUTKO-1) and was found to be capable of spontaneous as well as induced EA and VCA expression. Both DUTKO-1 and DITRUD-1 were similar to Daudi in their induction profile in respect to a very low response to TPA.
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PMID:Human lymphoma-lymphoma hybrids and lymphoma-leukemia hybrids. II. Epstein-Barr virus induction patterns. 627 88

Mouse monoclonal antibody to HTLV p19 was used to locate HTLV p19 on the surface of cells and virions by immunofluorescence microscopy (IFM) and immunoelectron microscopy (IEM). When HTLV-producing cells HUT 102 (B2 clone), MT-2 and strain A were used as target cells, HTLV p19 was detected on the surface of cells and virions as spots or small sectors by both IFM and IEM. Cells infected with animal type-C retroviruses, e.g., gibbon ape leukemia virus, simian sarcoma virus, feline leukemia virus, and Gross murine leukemia virus, were completely negative for HTLVp19 expression. Other human T cells not producing HTLV, including HUT78 and HSB2-0, immature or pre-T cells (Molt-3) derived from leukemia patients, and fresh peripheral blood T cells from healthy persons, were also negative. In addition, B cells including Rob-B, IM-9, Raji, and BT-1 did not react with the monoclonal antibody to HTLV p19. In the light of the presence of HTLV p19 in the periphery of acetone-fixed HTLV-producing cells as shown by IFM, it seems most likely that HTLV p19 is an internal antigen of HTLV with part of its structure protruding out of the viral and cell membrane. The monoclonal antibody to HTLV p19 did not lyse HTLV-producing cells in the presence of complement, as expected, because the antibody is an IgG1. Antibody-dependent cell-mediated cytotoxicity was also studied by the 51Cr-release assay. No cytotoxicity was observed. Although HTLV p19 does not contribute to the destruction of malignant T cells for treatment and/or virions for prophylaxis, this protein is an important marker for diagnosis of HTLV infection. The patterns of HTLV p19 expression described above were exactly the same for American HTLV-producing HUT 102 (B2 clone), for strain A cells and for Japanese HTLV-producing MT-2 cells. These results further substantiate the close relationship of the Japanese and American HTLV isolates.
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PMID:Location of human T-cell leukemia virus (HTLV) p19 antigen on virus-producing cells. 631 98


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